Chapter 3 The health effects of active smoking

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Winnall, WR|Hurley, S|Greenhalgh, EM|Winstanley, MH. 3.5.1 Oral, nasal and sinus cancers. In Greenhalgh, EM|Scollo, MM|Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne : Cancer Council Victoria; 2019. Available from https://www.tobaccoinaustralia.org.au/chapter-3-health-effects/3-5-other-cancers/3-5-1-oral-nasal-and-sinus-cancers
Last updated: January 2025

3.5.1 Oral, nasal and sinus cancers

Oral cancer describes cancers starting in or near the mouth. These include cancers that start in the floor of the mouth, cheeks, gums, roof of the mouth, lips, tongue, tonsils, or salivary glands. In terms of the population statistics presented here, cancer in the oropharynx (part of the throat behind the mouth) is also grouped with oral cancers,1 but the association between smoking and oropharyngeal cancer is discussed in Section 3.5.2. About 90% of these cancers are described as squamous cell carcinomas, which arise from the cells lining the surfaces of the mouth and nose.2

Oral cancer is relatively common in Australia, with an estimated 4,283 people diagnosed in 2024.1 An estimated 853 people died from oral cancer in 2024 in Australia.3 The chance of surviving for at least five years after diagnosis was 76.5%, based on data over the period 2016–2020.4 The 5-year survival rate for oral cancer has gradually increased from 70.6% (1991–1995) to 76.5% (2016–2020).4 Among oral cancer subsets, the five-year survival rate was highest for lip cancer (93.5%) and lowest for oral cancers arising in the gums, floor or roof of the mouth (63.9%).4

Nasal and sinus cancers are rare in Australia. In 2024, there were an estimated 130 people diagnosed with nasal cancer and three people who died from it.1,3 The chances of surviving for 5 years after diagnosis with nasal cancer were 72.0% (in 2016–2020).4 Cancer registry data indicates that 106 people were diagnosed with sinus cancer and 39 who died from it in 2024.1,3 The 5-year survival rate for sinus cancer was 55.0% (in 2016–2020).4  

The lived experience for people with oral cancer is one of difficulty. Treatments include surgery to remove part of the mouth, tongue or lips, as well as radiotherapy, chemotherapy, and other drug therapies. The effects of treatment can make it difficult for a person to eat, damage their sense of smell or taste, and change the look of a person’s face, leading to psychological effcts.5

3.5.1.1 Risk associated with smoking

Oral cancer

Smoking causes oral cancer.6,7 One meta-analysis of studies from 1961 to 2003 found that people who had ever smoked had a 3.4-fold higher risk of oral cancer compared to non-smokers.8

People who use other types of tobacco products, such as cigars, pipes, bidis and shisha, also have a higher risk of oral cancers than non-smokers (see Section 3.27). There is also evidence that use of smokeless tobacco increases the risk of oral cancer: meta-analyses have shown that smokeless tobacco users in South-East Asia had a 4.4-fold higher odds and in India had a 5.5-fold higher odds of oral cancer compared to those who did not use smokeless tobacco (see Section 18A.3).9,10 Further strengthening the evidence that smoking causes oral cancer are studies showing that smoking cessation leads to a reduction in the risk of oral cancer.11 Furthermore, people exposed to secondhand smoke also have a higher risk of oral, nasal and sinus cancer (see Section 4.10.1).

Nasal and sinus cancer

An extensive review by International Agency for Cancer (IARC) concluded that smoking causes cancer of the nasal cavity and paranasal sinuses.7 People who smoke have approximately double the odds of getting nasal cancer12,13 and 3-fold higher odds of sinus cancer.14

Oral potentially malignant disorders (OPMD)

Numerous abnormalities in the oral cavity are considered pre-cancerous conditions and collectively termed oral potentially malignant disorders (OPMD). These include oral leukoplakia, erythroplakia, proliferative verrucous leukoplakia, oral submucous fibrosis, and oral lichen planus. In some cases, these precancerous conditions progress to cancer. Smoking is considered the most important factor that promotes formation of some OPMDs and their progression to oral cancer (oral squamous cell carcinoma).15,16

3.5.1.2 How tobacco smoke causes oral, nasal and sinus cancers

The cells lining the mouth, nose and sinuses are usually the first to be exposed to tobacco smoke. Chemicals in tobacco smoke or from smokeless tobacco can directly access these cells through the mouth and nose. These chemicals also enter the bloodstream via the lungs and circulate to all parts of the body where they do damage, including to the mouth, nose and sinuses. Carcinogens and other toxic chemicals from tobacco smoke can damage DNA as well as disrupt various cellular processes, leading to the formation of cancer.

Damage to DNA in oral and nasal cells from exposure to carcinogens in tobacco smoke

The mechanisms by which smoking and tobacco exposure cause cancer are described in Section 3.3 and briefly summarised here. Carcinogens from tobacco and smoke are absorbed into cells where may interact with DNA (the part of a cell that contains the blueprint to create new cells). Sections of DNA bonded to a carcinogenic chemical are called DNA adducts. These DNA adducts lead to changes (mutations) in the sequence of genes, leading to changes in the function of cellular components such as proteins and microRNAs. DNA adducts also lead to breaks in the DNA and instability of chromosomes that results in changes to the copy numbers of specific genes – a common feature of many types of cancer. An accumulation of these changes culminates in dysregulation of cellular process and the uncontrolled cell proliferation that underlies cancer. Alternative mechanisms exist whereby carcinogens cause oxidative stress, epigenetic changes to DNA (which don’t change the DNA sequence) or hijack hormone and other signal transduction pathways, as described in Section 3.3.

Oral cancers are likely to be driven by carcinogens from smoke called PAHs (polycyclic aromatic hydrocarbons), NNK (4-(methylnitrosamino)-1(3-pyridyl)-1-butanone), and NNN ( N'-nitrosonornicotine).17 This conclusion is supported by a study from 2017 demonstrating that high levels of tobacco carcinogen-derived DNA damage in oral cells is an independent predictor of oral and head and neck cancer risk in smokers.18 Numerous studies have demonstrated that smokers have higher levels of DNA adducts in nasal and oral tissue samples than non-smokers.17 These include DNA adducts involving the carcinogens acrolein, crotonaldehyde, acrylonitrile and vinyl chloride.19 Such carcinogens promote DNA mutations and chromosomal changes, which are more numerous in the oral mucosa of smokers.20 For example, PAHs are predicted to cause mutations in the influential TP53 gene, found in oral tumours.17

Nasal cancers caused by smoking are likely to involve NNK, NNN, other nitrosamines and aldehydes.17 Chemicals from smoke, such as NNN, are capable of causing nasal cavity tumours in rodents.7

A study of squamous cell carcinomas found in head and neck cancers in general showed that tobacco-caused tumours had many common features of damage to these cells.21 Thirty five genes had DNA-adduct induced breaks in DNA and changes to the number of copies of specific genes — a common type of damage found in cancerous cells. The extent of the damage was related to the intensity of smoking (measured in pack-years).21

See Section 12.4.3 for more about the cancer-causing chemicals in tobacco smoke.

Disruption of cellular process that can lead to cancer

Exposure of cells to carcinogens and other toxic chemicals from cigarette smoke can lead to oxidative stress and oxidative damage. Oxidative stress occurs when damaging reactive oxygen species build up past a cell’s ability to detoxify them.22 Oxidative damage is associated with various stages in the development of cancer (carcinogenesis).23 Markers of oxidative stress are higher in the oral cells of people who smoke than in those of non-smokers.19

People who smoke have signs of lipid peroxidation (damage to fat molecules) in their oral cells.19,24 Lipid peroxidation can lead to the formation of damaging byproducts that are involved in cancer formation.  

Oral cells from people who smoke show evidence that the molecular pathways that can lead to cancer have been activated (“switched on”).25,26

3.5.1.3 Factors affecting risk

Intensity and duration of smoking

Oral, nasal and sinus cancers are often grouped with throat and voice box cancers under the term 'head and neck cancers'. The risk of getting any head and neck cancer increases with both the duration (how long) and intensity (how much per day) of smoking. Pooled analyses of 33 case–control studies predicted that duration of smoking had a stronger effect on the risk of head and neck cancers than the number of cigarettes smoked per day.27,28

A study that pooled data for oral and throat cancers also found that both intensity and duration of smoking increased the risks of these cancers, but that duration of smoking had a stronger effect than number of cigarettes per day.27

Alcohol consumption

Alcohol consumption is a risk factor for, and cause of, numerous cancers including oral cancer. Together, alcohol and tobacco are considered to be the two most important risk factors for head and neck cancers (cancers of the mouth, nose and sinuses plus the throat and voice box). Since people who smoke often drink, alcohol consumption levels affect the extent of risk associated with smoking.

The effects of smoking and alcohol are synergistic in relation to head and neck cancers (the combined effect of tobacco and alcohol exceeds the sum of their individual effects).6,7 A pooled analysis of 17 European and American case–control studies found that 4% of head and neck cancers were attributable to alcohol alone, 33% to tobacco alone and a further 35% were due to tobacco and alcohol combined.29

People who drink alcohol as well as smoke are at greater risk of oral cancer. In a pooled analysis of multiple studies, people who consumed alcohol and smoked has an almost 5-fold increased odds of getting oral cancer compared to people who abstained from both.29 The effects were dose-dependent: the odds of oral cancer was over 15-fold higher for people who drank three or more alcoholic drinks per day and smoked 20 or more cigarettes per day, compared to those who did not drink or smoke. For people who both consumed alcohol and smoked, 64% of oral cancers were attributable to these risk factors.29

The combined effects of alcohol and smoking also affected the location in which oral cancers occurred. People who both smoked and consumed alcohol were considerably more likely to have oral cancers in the floor of their mouth than oral cancer patients who did not smoke and drink.30

Human papilloma virus infection

Human papilloma virus (HPV) infection is a cause of cancer; it is suspected to cause nearly all cases of cervical cancer. HPV also infects the mouth and throat, putting people at risk of cancer in these regions.31

Smoking is estimated to cause an increased risk of head and neck cancers (oral, nasal and sinus, plus throat and voice box) by 2.7-fold for people with HPV infections and by 3-fold for people without HPV infections.32 The causal association between HPV infection and oropharyngeal cancer (in the throat behind the mouth, described in Section 3.5.2.3) is well established, however the association between HPV infection and oral cancer remains unclear. The low rates of HPV infection found in oral cancer cells and other issues with the current research cast doubt on whether HPV is driving the formation of oral cancer.33,34 

Smoking cessation

Smoking cessation reduces the risks of getting cancer in the oral cavity.11,35 Smoking cessation leads to a gradual decline in the excess risk of oral cancer. Cessation approximately halves the risks for oral cancer, compared with continued smoking, by 10 years after cessation, with further reduction over a longer period of abstinence.11,36 Cessation of smokeless tobacco use, in one study, lead to clinical resolution of many oral leukoplakia lesions (an oral potentially malignant disorder that can progress to cancer).37

3.5.1.4 Impact of smoking on prognosis

People who smoke when diagnosed with oral cancer are more likely to die sooner than people who are non-smokers and former smokers.38-40 For people treated with localised oral cancer, there is a greater risk that this cancer will return and spread for those who continue smoking compared to people who quit.38 People diagnosed with oral cancer who had a history of smoking and drinking alcohol are almost twice as likely to die from this cancer as non-drinkers/non-smokers.41

Smoking is associated with poor outcomes from head and neck cancers (oral, nasal, sinus, throat or voice box cancer). A 2019 meta-analysis showed that for people with head and neck cancers receiving radiotherapy, continued smoking was associated with lower overall survival, lower loco-regional control and higher risk of late toxicities.42 Studies of patients with head and neck cancer have shown poorer local-regional control,43,44 disease-free survival44 and overall survival39,43-45 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,46 disease-free survival43,46 and overall survival39,43,46,47 compared with those who quit.

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References

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Intro
Chapter 2