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Oral cancer risk factors

The key risk factors for oral cancer are discussed on this page. Oral cancer risk is also linked with age and sex, as shown on the incidence statistics page. Around 91% of oral and pharyngeal cancers were linked to lifestyle in the UK in 2010, it has been estimated, with a higher proportion in men (93%) than women (85%).1 The majority of these cases were caused by smoking.1

Meta-analyses and systematic reviews are cited where available, as they provide the best overview of all available research and most take study quality into account. Individual case-control and cohort studies are reported where such aggregated data are lacking.

Oral cancer risk factors overview

The International Agency for Research on Cancer (IARC) evaluates evidence on the carcinogenic risk to humans of a number of exposures including tobacco, alcohol, infections, radiation (UV and ionising), occupational exposures, and medications.2 The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) evaluates evidence for other exposures including diet, overweight and obesity, and physical exercise.3 IARC and WCRF/AICR evaluations are the gold standard in cancer epidemiology. Their conclusions about oral cancer risk factors are shown in Table 4.1.1

Table 4.1: IARC and WCRF/AICR Evaluations of Oral Cancer Risk Factors

Increases risk ('sufficient' or 'convincing' evidence) May increase risk ('limited' or 'probable' evidence) Decreases risk ('sufficient' or 'convincing' evidence) May decrease risk ('limited' or 'probable' evidence)

-

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Tobacco

Smoking

IARC classifies tobacco smoking as a cause of oral cavity, tonsil, pharynx and nasopharynx cancers.2 Smoking tobacco causes around 70% of oral and pharyngeal cancers in men, and around 55% in women in the UK, it is estimated.4

Current smokers have a three-fold increased risk of oral cavity cancer, compared with people who have never smoked, a meta-analysis showed.5 They also have nearly seven times the risk of pharyngeal cancer.5

Oral cavity cancer risk is both dose- and duration-dependent, a pooled analysis showed.6 It is almost 3 times higher in men and more than 4 times higher in women who have smoked the most cigarettes for the most years, compared with those who have smoked the least for the fewest years.6 Oropharynx cancer risk too is higher in the heaviest- and longest-smoking men (almost twice higher) and women (more than 3 times higher).6

Smoking cessation leads to a fall in risk, a pooled analysis showed.7 Between one and four years after cessation the risk of oral cavity cancer is 35% lower than that of a current smoker, and at 20 years or more after cessation the risk is reduced to that of a never-smoker.7 Oropharynx/Hypopharynx cancer risk reduces by around half within 5-9 years of smoking cessation, and is almost back to that of a never-smoker by 20 years or more.7

People who have only smoked pipes or cigars, rather than cigarettes, also have an increased risk of head and neck cancers (comprising oral cavity, pharynx and larynx), a pooled analysis showed.8 Those who only smoke cigars increase their risk by three-and-a-half times, and those who only smoke a pipe increase theirs by nearly four times.8 The risks increased with heavier or longer-term cigar or pipe use.8 People who smoke bidi (a type of south Asian handrolled cigarette) have around three times the risk of oral cancer compared with bidi never-smokers, a meta-analysis of south Asian studies showed.9 Risk of oropharyngeal cancer is not associated with marijuana smoking, a pooled analysis showed.67

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Environmental tobacco smoke

IARC classifies secondhand or environmental tobacco smoke (ETS) as a probable cause of pharynx cancer.2 Exposure to ETS increases oral and oropharyngeal cancer risk, a large case-control study showed.10 Never-smokers who have ever been exposed to ETS at home or work have an 87% higher risk, and those exposed in this way for 15 years or more have more than double the risk.10

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Smokeless tobacco

IARC classifies smokeless tobacco as a cause of oral cavity cancer.2 Oral cancer risk varies by geographical location, probably due to differences in the composition and format (e.g. chewing or inhaling nasally) of smokeless tobacco. Risk of oral cancer is more than doubled among smokeless tobacco users in the United States and Canada, increased five-fold in India and other Asian countries, and seven-fold in Sudan, but in the Nordic countries there was no such increase, a meta-analysis showed.11

IARC classifies betel quid with tobacco as a cause of oral cavity, tonsil and pharynx cancers, and betel quid without tobacco as a cause of oral cavity cancer.2 Betel quid without tobacco increases the risk of oral cancer in non-smokers by around three-and-a-half times, and in those who neither smoke nor drink by around 15 times, meta-analyses show.12,13,63 Betel quid with tobacco increases the risk of oral cancer in those who neither smoke nor drink by around seven times, a meta-analysis of studies from India (where tobacco is usually added to betel quid)64 showed.63 People who smoke tobacco, drink alcohol and chew betel have over 30 times the oral cancer risk compared with those who do none of these things.63

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Alcohol

IARC and WCRF/AIRC classify alcohol as a cause of oral cavity, tonsil and pharynx cancers.2,3 Alcohol drinking causes around 37% of oral and pharyngeal cancers in men, and around 17% in women in the UK, it is estimated.14

Every 1.5 units of alcohol consumed per day increases the risk of oral and pharyngeal cancer by 35% in men and 9% in women, a meta-analysis showed.15 Each 6 units daily increases the risk more than threefold (223% and 231% increase for men and women respectively).15 Overall, regular drinkers have around two-and-a-half times (155% increase) the risk of oral and pharyngeal cancer, compared with non-drinkers and occasional drinkers, a meta-analysis showed.15 The risk increase is greater for men (133%) than women (84%).15 Heavy drinking (around 6 units or more per day) increases the risk of oral and pharyngeal cancer more than fivefold (440%).15 Risk of secondary upper aerodigestive tracht (UADT, comprising oral cavity, pharynx, larynx, or oesophagus) in people with a previous UADT cancer is increased by 9% for every 1.25 units of alcohol consumed per day, a meta-analysis showed.66

Alcohol has a more pronounced effect on current smokers (192% increased risk of oral and pharyngeal cancers) than never/former smokers (32%), a meta-analysis showed.15 Heavy-drinking ever-smokers have almost seven-fold (567%) higher risk than heavy-drinking never-smokers (153%).15 Pooled analyses show a dose-response effect for oral cavity, oropharyngeal and hypopharyngeal cancers among ever-smokers,6 but among never-smokers the effect may be limited to oropharyngeal/hypopharyngeal cancer.16 Smokeless tobacco in conjunction with alcohol also increases oral cancer risk.17,18

Use of mouthwash containing alcohol is not associated with oral cancer risk, a meta-analysis showed.19

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Radiation

IARC classifies solar radiation as a probable cause of lip cancer.2 The possibility of residual confounding by tobacco use cannot be ruled out in some studies.20

IARC classifies X-radiation and Gamma radiation as causes of salivary gland cancer; and classifies radioiodines as probable causes.2 Early evidence on the effects of ionising radiation came from atomic bomb survivors,21 though most modern evidence comes from studies of people exposed to diagnostic or therapeutic medical radiation. Survivors of childhood cancer and Hodgkin lymphoma have a higher risk of salivary gland cancer (39-fold and 17-fold respectively), compared with the general population, due to radiation treatment for the primary tumour.22,23 Thyroid cancer survivors have between three and 11 times the population risk of salivary gland cancer, attributable to treatment with radioiodines.24,25

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Infections

Human papillomavirus (HPV)

IARC classifies human papillomavirus type 16 (HPV-16) as a cause of oral cavity, tonsil and pharynx cancers, and HPV-18 as a probable cause of oral cancer.2 HPV infection causes around 8% of oral cavity cancers and around 14% of oropharyngeal cancers in the UK, it is estimated.26

Around 4 in 10 (40%) oropharyngeal cancer cases in Europe are HPV-positive, a meta-analysis shows.27 The oropharyngeal cancer HPV prevalence rate appears to have increased over time, reaching over 70% in data from 2005 onwards.27 For non-oropharyngeal head and neck cancers (including oral cavity, hypopharynx and larynx), prevalence in European cases is around a quarter (24%), with no significant increase over time.27 HPV infection usually occurs through sexual activity, accordingly people with a higher number of past sex partners (particularly oral sex partners), or who started having sex at a younger age, have an increased risk of oropharyngeal, tonsil, and base of tongue cancers, a pooled analysis showed.28

Epstein-Barr virus (EBV)

IARC classifies EBV as a cause of nasopharynx cancer.2 EBV infection is present in 90% of nasopharyngeal cancer cases in the UK, it is estimated, equating to around 6% of oral cavity and pharynx cancers overall.29

HIV/AIDS

People with HIV/AIDS have around double the risk of oral, oropharyngeal and pharyngeal cancers, compared with the general population, meta-analyses have shown.30,31 There is a positive association between HIV and HPV infection.32

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Immune system

Oral cavity and pharynx cancer risk is 2-5 times higher in organ transplant recipients compared with the general population, a meta-analysis and several large cohort studies have shown.30,33,34 Lip cancer risk is particularly elevated in transplant recipients,30,33,34 perhaps associated with persistent HPV infection and increased sensitivity to UV radiation due to immunosuppressant medication.35

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Medical conditions and treatments

Oral conditions

Oral dysplasia including oral leukoplakia and erythroplakia can precede oral squamous cell carcinoma. These conditions are thought to be rare in the UK, but evidence on incidence is lacking.36 In an estimated 12% of cases these conditions will transform into cancer, a meta-analysis showed.37

Patients with periodontal (gum) disease are at 2.6 times the risk of head and neck cancers, a meta-analysis has shown.61 People who lose 6 or more teeth have at least 60% increased risk of head and neck cancer, a meta-analysis showed; the risk increases with the number of teeth lost.62

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Allergic rhinitis

Men with allergic rhinitis appear to have around half the risk oral and pharyngeal cancers, compared with non-allergic men, while allergy in women is not associated with oral or pharyngeal cancer risk, a meta-analysis showed.58 However, methods of allergy assessment and possible confounding by smoking status mean these findings may not be robust.

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Medications

IARC classifies hydrochlorothiazide, an antihypertensive medication which has photosensitising effects, as a probable cause of lip cancer.2 A US cohort study showed white people who used hydrochlorothiazide for five years or more had a fourfold increased risk of lip cancer, compared with never-users.38

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Previous cancer

Increased risk of oral cancer following a previous cancer diagnosis is probably due to a combination of shared aetiological factors (e.g. smoking or HPV) and the effect of radiotherapy treatment for the first cancer. People with a previous head and neck cancer (including tongue, mouth, pharynx, and larynx) have between 12- and 16-fold increased risk of subsequent head and neck cancer, a pooled analysis showed.39 Survivors of squamous cell carcinoma of the oesophagus have an almost seven-fold increase in risk of oral cavity and pharynx cancers.40 People with a previous lung cancer have between 1.5 and 5.7 times the general population risk of developing head and neck cancer, varying by patient sex and lung tumour histology.41 Women with previous cervical squamous cell carcinoma have an increased risk of mouth and pharynx cancers.42

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Family history and genetic conditions

A family history of head and neck cancer, particularly in a sibling, is associated with almost doubling (70% increase) of head and neck cancer risk, a pooled analysis showed.43 Genetic susceptibility and shared risk factors probably both play a part, as personal exposure to tobacco compounds this effect: alcohol and tobacco users with a family history of head and neck cancer have more than sevenfold increased risk. Family history of other tobacco-related cancers also increases the risk of head and neck cancer.

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Occupational exposures

Formaldehyde and wood dust are classified by IARC as causes of nasopharyngeal cancer (Table 4.1).2 An estimated 11% of pancreatic cancers in men in Great Britain, and around 2% in women, are linked to occupational exposure to formaldehyde or wood dust.44

Nasopharyngeal cancer death risk may not be associated with formaldehyde exposure, cohort studies have shown;47,69 however evidence is mixed.45

Nasopharyngeal cancer death risk may be 2.4 times higher in furniture and plywood workers, a pooled analysis showed;46 however evidence is mixed.47

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Asbestos and exposure to printing processes (which may entail exposure to polycyclic aromatic hydrocarbons and mineral oils) are classified by IARC as probable causes of pharynx cancer, based on limited evidence (Table 4.1).2

Oral and pharyngeal cancer risk is 25% higher in people exposed to asbestos, compared with the general population, a meta-analysis showed.48 

Oral and pharyngeal cancer risk is 14% higher in people exposed to polycyclic aromatic hydrocarbons.48

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Diet

IARC classifies salted fish (Chinese-style) as a cause of nasopharyngeal cancer.2 The association is probably due to nitrosamine, levels of which are higher in Chinese-style than other types of salted fish. People with the highest intakes of Chinese-style salted fish during childhood have around two-and-a-half times the risk of nasopharyngeal cancer in adulthood, a case-control study showed.49 However, salted fish intake was not associated with nasopharyngeal cancer risk at a population level, after controlling for tobacco use and vegetable intake, another study found.50

IARC and WCRF/AICR classify drinking hot maté, a traditional South American infused drink, as a cause of pharyngeal cancer.2,3 Maté users have around double the risk of oral and oropharyngeal cancer compared with non-users or low-users, a meta-analysis of case-control studies from Latin America showed.51 It remains unclear whether this is due to the hot temperature of the drink, or to some carcinogenic substances in the drink.51

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Height

Head and neck cancer risk is 9% lower per 10cm increase in height for men, and 14% lower per 10cm height for women, a pooled analysis showed.65

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Factors shown to decrease or have no effect on oral cancer risk

Diet

WCRF/AICR classifies consumption of non-starchy vegetables and fruits (not salted or pickled), and foods containing carotenoids, as possibly protective against mouth, pharynx and larynx cancers. Eating fewer than five portions (400g in total) of fruit and vegetables each day causes around 57% of oral and pharyngeal cancers in men, and around 54% in women in the UK, it is estimated.52 However, links between diet and oral cancer are considerably less certain than links with other risk factors, such as smoking and alcohol.1,4

People with the highest fruit intake have around half the risk of head and neck cancer, compared with people with the lowest fruit intake, a pooled analysis showed.53 And each portion of fruit consumed per day around halves the risk of oral cancer, as does each portion of vegetables, a meta-analysis showed.54

People who have ever used vitamin C supplements have a 24% reduced risk of head and neck cancer, and ever-users of calcium supplements have a 36% reduced risk, a pooled analysis shows; however clear dose-response effects were not observed for any supplements, therefore the association remains unclear.55

People who drink one cup of caffeinated coffee each day have a 4% lower risk of oral cavity and pharynx cancer compared with non-drinkers, and those who drink more than four cups daily have a 39% risk decrease, a pooled analysis showed.56 Black tea and decaffeinated coffee do not appear to be associated with oral cancer risk.56,68 Oral cancer risk may be slightly reduced by green tea consumption, a meta-analysis showed.68

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Physical activity

Recreational physical activity at moderate or high levels is associated with a 26-47% reduction in oral cancer risk, and a 33-42% reduction in pharyngeal cancer risk, compared with very low levels or no recreational physical activity at all, a pooled analysis showed. The beneficial effects of recreational physical activity on head and neck cancer risk seem to be stronger in males, people aged 45 or younger, and ever-smokers and ever-drinkers.57

Overweight and obesity

A meta-analysis of case-control studies found that, compared with healthy-weight people, overweight and obese people had under half the risk of oral cancer, and underweight people had more than double the risk.59 However, the design of the included studies means residual confounding by smoking and possible reverse causality (weight loss caused by as-yet undiagnosed oral cancer) cannot be ruled out. A prospective cohort study found no association between body mass index and risk of oral cavity, oropharynx or hypopharynx cancers.60

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References for oral cancer risk factors

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Updated: 31 October 2013