Head and neck cancers risk factors

Prevention

Preventable cases of head and neck cancer, UK

Smoking

Head and neck cancer cases linked to exposure to tobacco smoke, UK

Alcohol

Head and neck cancer cases linked to alcohol consumption, UK

 

HPV

Head and neck cancer cases linked to human papillomavirus (HPV) infection, UK

91% (93% in males and 85% in females) of oral cancer cases each year in the UK are linked to major lifestyle and other risk factors.[1]

93% (93% in males and 91% in females) of laryngeal cancer cases each year in the UK are linked to major lifestyle and other risk factors.[1]

Head and neck cancer risk is associated with a number of risk factors.[2,3]

Head and Neck Cancer Risk Factors

  Increases risk Decreases risk
'Sufficient' or 'Convincing' evidence
  • Alcoholic drinks [a,b,g]
  • Betel quid with tobacco [a,b]
  • Betel quid without tobacco [a]
  • Human papillomavirus (HPV) type 16 [a,b,c]
  • Tobacco smoking [a,b,g]
  • Smokeless tobacco [a]
  • X-radiation, gamma-radiation [d]
  • Epstein-Barr virus (EBV) [e]
  • Formaldehyde [e]
  • Strong inorganic acid mists [g]
  • Asbestos [g]
  • Salted fish, Chinese-style [e,i]
  • Wood dust [e]
 
'Limited' or 'probable' evidence
  • HPV type 16 [g]
  • HPV type 18 [a]
  • Hydrochlorothiazide [f]
  • Sulphur mustard (mustard gas) [g]
  • Solar radiation [f]
  • Radioiodines, including Iodine-131 [d]
  • Asbestos (all forms) [b]
  • Printing processes [b]
  • Working in rubber production [g]
  • Environmental tobacco smoke [b, g]
  • Non-starchy vegetables [h,j]
  • Fruits [h,j]
  • Foods containing carotenoids [g]
International Agency for Research on Cancer (IARC) and World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) classifications.
 
a Oral cavity; b Pharynx; c Tonsil; d Salivary gland; e Nasopharynx; f Lip; g Larynx; h WCRF/AICR classification is for mouth, pharynx and larynx; i IARC classifies evidence on Chinese-style salted fish as sufficient, WCRF/AICR classifies evidence on Cantonese-style salted fish as probable; j not salted or pickled
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Tobacco smoking is classified by the International Agency for Research on Cancer (IARC) as a cause of oral cavity, pharynx, nasopharynx and laryngeal cancers.[1] An estimated 65% (70% in males and 55% in females) of oral and pharyngeal cancers and 79% of laryngeal cancers in the UK are linked to tobacco smoking.[2]

Oral cavity cancer risk is 91% higher in current smokers compared with never-smokers, a cohort study showed.[3] Pharyngeal cancer risk is 3 times higher in current smokers compared with never-smokers, a meta-analysis showed.[4] Nasopharyngeal cancer risk is 47-95% higher in current smokers compared with never-smokers, meta-analyses have shown.[4,5] Laryngeal cancer risk is 8.3 times higher in people who have ever smoked cigarettes compared with those who have never done so, a pooled analysis of case-control studies showed.[6]

Head and neck (including oral cavity, pharynx, hypopharynx, oropharynx, and larynx) cancer risk increases with amount and duration of cigarette smoking.[6] Oral cavity cancer risk in men is almost 3 times higher in those who have smoked the most cigarettes for the most years, compared with those who have smoked the least for the fewest years, a pooled analysis showed.[7] Oral cavity cancer risk in women is more than 4 times higher in the heaviest- and longest-smokers versus the lightest- and shortest-smokers.[7] Oropharynx cancer risk in men is almost twice as high in the heaviest- and longest-smokers versus the lightest- and shortest-smokers.[7] Oropharynx cancer risk in women is more than 3 times higher in the heaviest- and longest-smokers versus the lightest- and shortest-smokers.[7]

Tobacco-associated laryngeal cancer risk may vary with specific site of cancer within the larynx, with a stronger association for supraglottis than glottis cancers.[8]

References

  1. International Agency for Research on Cancer. List of Classifications by cancer sites with sufficient or limited evidence in humans, Volumes 1 to 117*. Accessed January 2017.
  2. Parkin DM. Tobacco-attributable cancer burden in the UK in 2010. Br J Cancer 2011; 105 (S2):S6-S13.
  3. Maasland DH, van den Brandt PA, Kremer B, at al. Alcohol consumption, cigarette smoking and the risk of subtypes of head-neck cancer: results from the Netherlands Cohort Study. BMC Cancer. 2014 Mar 14;14:187.
  4. Gandini S, Botteri E, Iodice S, et al. Tobacco smoking and cancer: a meta-analysis. Int J Cancer 2008; 122(1):155-64.
  5. Xue WQ, Qin HD, Ruan HL, et al. Quantitative association of tobacco smoking with the risk of nasopharyngeal carcinoma: a comprehensive meta-analysis of studies conducted between 1979 and 2011. Am J Epidemiol. 2013 Aug 1;178(3):325-38.
  6. Wyss A, Hashibe M, Chuang SC, et al. Cigarette, cigar, and pipe smoking and the risk of head and neck cancers: pooled analysis in the International Head and Neck Cancer Epidemiology Consortium. Am J Epidemiol 2013;178(5):679-90.
  7. Lubin JH, Muscat J, Gaudet MM, et al. An examination of male and female odds ratios by BMI, cigarette smoking, and alcohol consumption for cancers of the oral cavity, pharynx, and larynx in pooled data from 15 case-control studies. Cancer Causes Control 2011;22(9):1217-31.
  8. Muscat JE, Liu HP, Livelsberger C, et al. The nicotine dependence phenotype, time to first cigarette, and larynx cancer risk. Cancer Causes Control 2012; 23(3):497-503.
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Oral cavity cancer risk is 35% lower in ex-smokers who quit 1-4 years previously, compared with current smokers, a pooled analysis showed.[1] Oral cavity cancer risk is no higher in ex-smokers who quit 20+ years previously, compared with never-smokers.[1]

Oropharynx/hypopharynx cancer risk is 49% lower in ex-smokers who quit 5-9 years previously, compared with current smokers. Oropharynx/Hypopharynx cancer risk is no higher in ex-smokers who quit 20+ years previously, compared with never-smokers.[1]

Laryngeal cancer risk in ex-smokers compared with continuing smokers is 30% lower after 1-4 years of non-smoking, and 64% lower after 10-19 years, a pooled analysis of case-control studies showed.[2] Laryngeal cancer risk is higher in ex-smokers than never-smokers for up to 20 years after smoking cessation.[2]

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Head and neck cancer (comprising oral cavity, pharynx and larynx) risk is 3.5 times higher in cigar-only smokers compared with never-smokers, a pooled analysis showed.[1] Head and neck cancer risk is nearly 4 times higher in pipe-only smokers compared with never-smokers. Risk increases with heavier or longer-term cigar or pipe use.[1]

Laryngeal cancer risk among people who have never smoked cigarettes is higher in those who have ever smoked cigars or a pipe, compared with never-users of these products.[1]

Oral cancer risk is around 3 times higher in bidi smokers compared with bidi never-smokers, a meta-analysis of south Asian studies showed.[2]

Head and neck cancer risk is associated with waterpipe tobacco smoking (smoking flavoured tobacco through a long pipe attached to a water bowl), a meta-analysis from mainly African and Asian studies showed; however confounding by cigarette smoking is possible.[3]

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Secondhand or environmental tobacco smoke (ETS) is classified by the International Agency for Research on Cancer (IARC) as a probable cause of pharyngeal and laryngeal cancers, based on limited evidence.[1]

Oral and oropharyngeal cancer risk is 87% higher in never-smokers who have ever been exposed to ETS at home or work, compared with unexposed never-smokers, a case-control study showed.[2] Oral and oropharyngeal cancer risk is more than twice higher in never-smokers exposed to ETS at home or work for 15+ years, compared with unexposed never-smokers.[2]

Laryngeal cancer risk may only be higher in people exposed to environmental tobacco smoke for many years, case-control studies have shown; evidence is limited by small numbers of laryngeal cancer cases in never-smokers.[2-4]

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Smokeless tobacco is classified by the International Agency for Research on Cancer (IARC) as a cause of oral cavity cancer.[1] Betel quid with tobacco is classified by IARC as a cause of oral cavity and pharynx cancers, and betel quid without tobacco as a cause of oral cavity cancer.[1]

Oral cancer risk among South Asians (who comprise the majority of smokeless tobacco users globally) is 5-7 times higher in smokeless tobacco users versus non-users, meta-analyses have shown.[2,3] Gum and oral cavity cancer risk may be higher in never smokers who have ever used nasal snuff or chewing tobacco, compared with non-users, a meta-analysis showed.[4]

The association between smokeless tobacco use and oral cancer risk varies by country probably due to differences in smokeless tobacco composition and format (e.g. chewing or inhaling nasally).[5]

Oral cancer risk in non-smokers is 3.5 times higher in betel quid without tobacco users compared with non-users, meta-analyses have shown.[6-8] Oral cancer risk in non-smokers and non-drinkers is around 15 times higher in betel quid without tobacco users compared with non-users.[6-8]

Oral cancer risk in non-smokers and non-drinkers is around 7 times higher in betel quid with tobacco users compared with non-users, a meta-analysis of studies from India (where tobacco is usually added to betel quid[9]) showed.[8] Oral cancer risk in smokers and drinkers is over 30 times higher in betel quid with tobacco users compared with non-users.[8]

References

  1. International Agency for Research on Cancer. List of Classifications by cancer sites with sufficient or limited evidence in humans, Volumes 1 to 117*. Accessed January 2017.
  2. Khan Z, Khan Z, Tönnies J, Müller S. Smokeless tobacco and oral cancer in South Asia: a systematic review with meta-analysis. J Cancer Epidemiol 2014;2014:394696.
  3. Gupta B, Johnson NW. Systematic review and meta-analysis of association of smokeless tobacco and of betel quid without tobacco with incidence of oral cancer in South Asia and the Pacific. PLoS One 2014;9(11):e113385.
  4. Wyss AB, Hashibe M, Lee YA, et al. Smokeless Tobacco Use and the Risk of Head and Neck Cancer: Pooled Analysis of US Studies in the INHANCE Consortium. Am J Epidemiol. 2016 Oct 15.
  5. Boffetta P, Hecht S, Gray N , et al. Smokeless tobacco and cancer. Lancet Oncol 2008; 9(7):667-75.
  6. Thomas SJ, Bain CJ, Battistutta D, et al. Betel quid not containing tobacco and oral cancer: A report on a case-control study in Papua New Guinea and a meta-analysis of current evidence. Int J Cancer 2007; 120(6):1318-23.
  7. Song H, Wan Y, Xu YY. Betel Quid Chewing Without Tobacco: A Meta-analysis of Carcinogenic and Precarcinogenic Effects. Asia Pac J Public Health 2013. doi: 10.1177/1010539513486921.
  8. Petti S, Masood M, Scully C. The magnitude of tobacco smoking-betel quid chewing-alcohol drinking interaction effect on oral cancer in South-East Asia. A meta-analysis of observational studies. PLoS One 2013;8(11):e78999.
  9. Jacob BJ, Straif K, Thomas G, et al. Betel quid without tobacco as a risk factor for oral precancers. Oral Oncol 2004;40(7):697-704.
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Alcoholic drinks are classified by the International Agency for Research on Cancer (IARC) and the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) as a cause of oral cavity, pharyngeal and laryngeal cancers.[1,2] An estimated 30% (37% in males and 17% in females) of oral and pharyngeal cancers, and an estimated 25% (27% in males, 12% in females) of laryngeal cancers in the UK are linked to alcohol drinking.[3]

Oral and pharyngeal cancer risk is 81% higher in people who consume around 12.5-50g (1.5-6 units) of alcohol per day, and 5 times higher in those who consume 50g+ (6+ units) of alcohol per day, compared with non- or occasional drinkers, a meta-analysis showed.[4] Oral and pharyngeal cancer risk is 2.5 times higher in regular drinkers compared with non- and occasional drinkers, a meta-analysis showed.[5]

Laryngeal cancer risk is 49% higher in people who consume around 12.5-50g (1.5-6 units) of alcohol per day, and 2.4 times higher in those who consume 50g+ (6+ units) of alcohol per day, compared with non- or occasional drinkers, a meta-analysis showed.[4] Laryngeal cancer risk is not associated with drinking less than around 1.5 units of alcohol per day,[4,6] but beyond this level, risk increases with higher alcohol intake.[4,6]

Laryngeal cancer risk is substantially higher in people who both smoke tobacco and drink alcohol, meta- and pooled analyses show; the effect of these two behaviours together is greater than the sum of their individual effects.[7,8]

Oral and pharyngeal cancer risk is almost tripled in alcohol drinkers who currently smoke tobacco, while it is 32% higher in alcohol drinkers who do not currently smoke, both compared with never-drinkers, a meta-analysis showed.[9] Oral cavity, oropharyngeal and hypopharyngeal cancer risk increases with amount of alcohol consumed among ever-smokers,[10] but among never-smokers the effect may be limited to oropharyngeal/hypopharyngeal cancer, pooled analyses have shown.[9] Oral cancer risk is higher in alcohol drinkers who use smokeless tobacco, compared with alcohol drinkers who do not use smokeless tobacco.[11,12]

Oral cancer risk is not associated with use of alcohol-containing mouthwash, a meta-analysis showed.[13]

Alcohol-associated laryngeal cancer risk may vary with specific site of cancer within the larynx, with a stronger association for supraglottis than glottis cancers.[14]

Laryngeal cancer risk in ex-drinkers compared with continuing drinkers decreases by 2% per year of non-drinking, a meta-analysis showed.[15] Laryngeal cancer risk is higher in ex-drinkers than never-drinkers for around 35 years after drinking cessation.[15]

References

  1. International Agency for Research on Cancer. List of Classifications by cancer sites with sufficient or limited evidence in humans, Volumes 1 to 117*. Accessed January 2017.
  2. World Cancer Research Fund / American Institute for Cancer Research. Continuous Update Project Findings & Reports. Accessed January 2017.
  3. Parkin DM. Cancers attributable to consumption of alcohol in the UK in 2010. Br J Cancer 2011; 105 (S2):S14-S18.
  4. Bagnardi V, Rota M, Botteri E, et al. Alcohol consumption and site-specific cancer risk: a comprehensive dose-response meta-analysis. Br J Cancer. 2015 Feb 3;112(3):580-93.
  5. Turati F, Garavello W, Tramacere I, et al. A meta-analysis of alcohol drinking and oral and pharyngeal cancers: results from subgroup analyses. Alcohol Alcohol 2013;48(1):107-18.
  6. Islami F, Tramacere I, Rota M. Alcohol drinking and laryngeal cancer: overall and dose-risk relation--a systematic review and meta-analysis. Oral Oncol 2010;46(11):802-10.
  7. Hashibe M, Brennan P, Chuang SC, 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 Epidemiol Biomarkers Prev 2009;18(2):541-50.
  8. Zeka A, Gore R, Kriebel D. Effects of alcohol and tobacco on aerodigestive cancer risks: a meta-regression analysis. Cancer Causes Control 2003;14(9):897-906.
  9. Hashibe M, Brennan P, Benhamou S, et al. Alcohol drinking in never users of tobacco, cigarette smoking in never drinkers, and the risk of head and neck cancer: pooled analysis in the International Head and Neck Cancer Epidemiology Consortium. J Natl Cancer Institute 2007; 99(10):777-89.
  10. 1Lubin JH, Muscat J, Gaudet MM, et al. An examination of male and female odds ratios by BMI, cigarette smoking, and alcohol consumption for cancers of the oral cavity, pharynx, and larynx in pooled data from 15 case-control studies. Cancer Causes Control 2011;22(9):1217-31.
  11. Znaor A, Brennan P, Gajalakshmi V, et al. Independent and combined effects of tobacco smoking, chewing and alcohol drinking on the risk of oral, pharyngeal and esophageal cancers in Indian men. Int J Cancer 2003; 105(5):681-6.
  12. Lin WJ, Jiang RS, Wu SH, et al. Smoking, alcohol, and betel quid and oral cancer: a prospective cohort study. J Oncol 2011;2011:525976.
  13. Gandini S, Negri E, Boffetta P, et al. Mouthwash and Oral Cancer Risk Quantitative Meta-analysis of Epidemiologic Studies. Ann Agric Environ Med 2012;19(2):173-80.
  14. La Vecchia C, Zhang ZF, Altieri A. Alcohol and laryngeal cancer: an update. Eur J Cancer Prev 2008;17(2):116-24.
  15. Ahmad Kiadaliri A, Jarl J, Gavriilidis G, et al. Alcohol drinking cessation and the risk of laryngeal and pharyngeal cancers: a systematic review and meta-analysis. PLoS One 2013;8(3):e58158.
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X-radiation and Gamma radiation are classified by the International Agency for Research on Cancer (IARC) as causes of salivary gland cancer; and radioiodines as probable causes, based on limited evidence.[1]

Salivary gland cancer risk is higher in survivors of childhood cancer, Hodgkin lymphoma, and thyroid cancer, compared with the general population, cohort studies have shown; this is due to radiation treatment (radiotherapy or radioiodines) for the primary tumour.[2-5]

Oral cancer risk is higher in atomic bomb survivors compared with the general population.[6]

References

  1. International Agency for Research on Cancer. List of Classifications by cancer sites with sufficient or limited evidence in humans, Volumes 1 to 117*. Accessed January 2017.
  2. Boukheris H, Stovall M, Gilbert ES, et al. Risk of salivary gland cancer after childhood cancer: a report from the Childhood Cancer Survivor Study. Int J Radiat Oncol Biol Phys 2013;85(3):776-83.
  3. Boukheris H, Ron E, Dores GM, et al. Risk of radiation-related salivary gland carcinomas among survivors of Hodgkin lymphoma: a population-based analysis. Cancer 2008;113(11):3153-9.
  4. Sandeep TC, Strachan MW, Reynolds RM, et al. Second primary cancers in thyroid cancer patients: a multinational record linkage study. J Clin Endocrinol Metab 2006;91(5):1819-25.
  5. Iyer NG, Morris LG, Tuttle RM, et al. Rising incidence of second cancers in patients with low-risk (T1N0) thyroid cancer who receive radioactive iodine therapy. Cancer 2011;117(19):4439-46.
  6. Saku T, Hayashi Y, Takahara O, et al. Salivary gland tumors among atomic bomb survivors, 1950-1987. Cancer 1997;79(8):1465-75.
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Solar radiation is classified by the International Agency for Research on Cancer (IARC) as a probable cause of lip cancer, based on limited evidence.[1] Confounding by tobacco use is possible.[2]

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Human papillomavirus (HPV) Open a glossary item type 16 is classified by the International Agency for Research on Cancer (IARC) as a cause of oral cavity, tonsil and pharyngeal cancers.[1] HPV type 16 is classified by IARC as a probable cause of laryngeal cancer, and HPV type 18 is classified as a probable cause of oral cavity cancer, based on limited evidence.[1] An estimated 8% of oral cavity cancers, 14% of oropharyngeal cancers, and 11% of laryngeal cancers in the UK are linked to HPV infection.[2]

73% of oropharyngeal cancer cases in Europe are HPV-positive Open a glossary item, a meta-analysis showed; this proportion has increased over time.[3] 12% of oral cavity, hypopharynx and larynx cancer cases in Europe are HPV-positive, with no change over time.[3]

Oropharyngeal, tonsil, and base of tongue cancer risk is higher in people with more past sexual partners (particularly oral sex partners), people who started having sex at a younger age, and men who have ever had sexual contact with men (base of the tongue only), a pooled analysis showed; this reflects the sexual route of HPV transmission.[4]

Laryngeal squamous cell carcinoma (SCC) risk is 5.4 times higher in people with HPV infection, a meta-analysis showed.[5] Laryngeal cancer risk is higher for HPV type 16 than HPV type 18.[5]

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Epstein-Barr virus (EBV) is classified by the International Agency for Research on Cancer (IARC) as a cause of nasopharynx cancer.[1] An estimated 90% of nasopharyngeal cancer cases in the UK are EBV-positive.[2]

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Oral, oropharyngeal and pharyngeal cancer risk is around twice higher in people with HIV Open a glossary item/AIDS Open a glossary item, compared with the general population, meta-analyses have shown.[1,2] This may reflect higher rates of Human papillomavirus (HPV) Open a glossary item infection in people with HIV.[3]

Laryngeal cancer risk is 50-172% higher in people with HIV versus those without, meta-analyses have shown.[1,2] This may reflect higher rates of smoking and HPV infection in people with HIV.[1,2]

References

  1. Grulich AE, van Leeuwen MT, Falster MO, et al. Incidence of cancers in people with HIV/AIDS compared with immunosuppressed transplant recipients: a meta-analysis. Lancet 2007; 370(9581):59-67.
  2. Shiels MS, Cole SR, Kirk GD, et al. A meta-analysis of the incidence of non-AIDS cancers in HIV-infected individuals. J Acquir Immune Defic Syndr 2009;52(5):611-22.
  3. Houlihan CF, Larke NL, Watson-Jones D, et al. Human papillomavirus infection and increased risk of HIV acquisition. A systematic review and meta-analysis. AIDS 2012;26(17):2211-22.
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Laryngeal cancer risk is twice as high in people with Helicobacter pylori (H. pylori) Open a glossary item infection versus those without, a meta-analysis showed.[1]

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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.[1-4] Lip cancer risk is particularly elevated in transplant recipients,[1-4] perhaps associated with persistent human papillomavirus (HPV) Open a glossary iteminfection and increased sensitivity to ultraviolet (UV) Open a glossary item radiation due to immunosuppressant medication.[5]

Laryngeal cancer risk is 1.6-2 times higher in organ transplant recipients compared with the general population, a meta-analysis and cohort study have shown.[1,2] This may reflect higher rates of HPV   infection in organ transplant recipients.[1]

References

  1. Grulich AE, van Leeuwen MT, Falster MO, et al. Incidence of cancers in people with HIV/AIDS compared with immunosuppressed transplant recipients: a meta-analysis. Lancet 2007; 370(9581):59-67.
  2. Engels EA, Pfeiffer RM, Fraumeni JF Jr, et al. Spectrum of cancer risk among US solid organ transplant recipients. JAMA 2011;306(17):1891-901.
  3. Krynitz B, Edgren G, Lindelöf B, et al. Risk of skin cancer and other malignancies in kidney, liver, heart and lung transplant recipients 1970 to 2008 - a Swedish population-based study. Int J Cancer 2013;132(6):1429-38.
  4. Liu Q, Yan L, Xu C, et al. Increased incidence of head and neck cancer in liver transplant recipients: a meta-analysis. BMC Cancer 2014;14:776.
  5. van Leeuwen MT, Grulich AE, McDonald SP, et al. Immunosuppression and other risk factors for lip cancer after kidney transplantation. Cancer Epidemiol Biomarkers Prev 2009;18(2):561-9.
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An estimated 12% of people with oral dysplasia (including oral leukoplakia and erythroplakia) develop oral cancer, a meta-analysis showed.[1]

Head and neck cancer risk is 2.6 times higher in people with periodontal (gum) disease, a meta-analysis showed.[2] Head and neck cancer risk is at least 60% higher in people who lose 6+ teeth, a meta-analysis showed; risk increases with number of teeth lost.[3] Oral cancer risk is 42% higher in people who wear dentures versus those who do not, and is 4 times higher in people with ill-fitting dentures versus non denture-wearers, a meta-analysis showed.[4]

References

  1. Mehanna HM, Rattay T, Smith J, et al. Treatment and follow-up of oral dysplasia - a systematic review and meta-analysis. Head Neck 2009;31(12):1600-9.
  2. Zeng XT, Deng AP, Li C, et al. Periodontal disease and risk of head and neck cancer: a meta-analysis of observational studies. PLoS One 2013;8(10):e79017.
  3. Zeng XT, Luo W, Huang W, et al. Tooth loss and head and neck cancer: a meta-analysis of observational studies. PLoS One 2013;8(11):e79074.
  4. Manoharan S, Nagaraja V, Eslick GD. Ill-fitting dentures and oral cancer: a meta-analysis. Oral Oncol. 2014 Nov;50(11):1058-61.
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Hydrochlorothiazide (an antihypertensive with photosensitising effects) is classified by the International Agency for Research on Cancer (IARC) as a probable cause of lip cancer, based on limited evidence.[1]

Lip cancer risk among white people is 4 times higher in those using hydrochlorothiazide for 5+ years versus never-users, a cohort study showed.[2]

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Laryngeal cancer develops in 14% of people with laryngeal dysplasia, on average around 6 years after dysplasia diagnosis, a meta-analysis showed.[1] Laryngeal cancer risk among people with laryngeal dysplasia is higher in those with more severe dysplasia.[1]

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Head and neck cancer (including tongue, mouth, pharynx, and larynx) risk is 12-16 times higher in people with a previous head and neck cancer, a pooled analysis showed.[1]

Oral cancer (definitions vary between studies) risk is higher in survivors of oesophageal squamous cell carcinoma (SCC) Open a glossary item, lung cancer, or cervical SCC, compared with the general population, cohort studies have shown.[2-4] This may reflect the effect of treatment for the primary cancer, or shared lifestyle, environmental or genetic risk factors.

Laryngeal cancer risk is 6.1 times higher in head and neck cancer (non-larynx) survivors, a pooled analysis of cancer registry data showed.[5] Laryngeal cancer risk is higher in survivors of several other cancer types including lung, oesophageal, bladder, and cervical squamous cell carcinoma.[2, 4, 6, 7] This may reflect shared risk factors, e.g. tobacco, alcohol and Human papillomavirus (HPV) Open a glossary item.

Oral cavity, pharynx and larynx cancer risk among survivors of upper aerodigestive tract cancer is 2.2 times higher in those with the highest alcohol intake versus those with the lowest, a meta-analysis showed.[8]

References

  1. Bosetti C, Scelo G, Chuang SC. High constant incidence rates of second primary cancers of the head and neck: a pooled analysis of 13 cancer registries. Int J Cancer 2011;129(1):173-9.
  2. Chuang SC, Hashibe M, Scelo G, et al. Risk of second primary cancer among esophageal cancer patients: a pooled analysis of 13 cancer registries. Cancer Epidemiol Biomarkers Prev 2008; 17(6):1543-9.
  3. Chuang SC, Scélo G, Lee YC, et al. Risks of second primary cancer among patients with major histological types of lung cancers in both men and women. Br J Cancer 2010;102(7):1190-5.
  4. Chaturvedi AK, Kleinerman RA, Hildesheim A, et al. Second cancers after squamous cell carcinoma and adenocarcinoma of the cervix. J Clin Oncol 2009;27(6):967-73.
  5. Chuang SC, Scelo G, Tonita JM, et al. Risk of second primary cancer among patients with head and neck cancers: A pooled analysis of 13 cancer registries. Int J Cancer 2008;123(10):2390-6.
  6. Surapaneni R, Singh P, Rajagopalan K, et al. Stage I lung cancer survivorship: risk of second malignancies and need for individualized care plan. J Thorac Oncol 2012;7(8):1252-6.
  7. Jégu J, Colonna M, Daubisse-Marliac L, et al. The effect of patient characteristics on second primary cancer risk in France. BMC Cancer 2014;14:94.
  8. Druesne-Pecollo N, Keita Y, Touvier M, et al. Alcohol drinking and second primary cancer risk in patients with upper aerodigestive tract cancers: a systematic review and meta-analysis of observational studies. Cancer Epidemiol Biomarkers Prev 2014;23(2):324-31.
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Head and neck cancer risk is 70% higher in people with a family (particularly sibling) history of head and neck cancer, versus those without such history, a pooled analysis showed.[1] Head and neck cancer risk is higher in people with a family history of other tobacco-related cancers versus those without.[1] Head and neck cancer risk among alcohol and tobacco users is more than 7 times higher in those with a family history of the disease versus those without.[1] This indicates shared lifestyle and environmental factors contribute to the increased risk, as well as genetic risk factors.

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Strong inorganic acid mists are classified by the International Agency for Research on Cancer (IARC) as a cause of laryngeal cancer.[1]

An estimated 2% of laryngeal cancers in Great Britain are linked to occupational exposure to strong inorganic acid mists.[2]

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Exposure to asbestos is classified by IARC as a probable cause of pharyngeal cancer, based on limited evidence.[1]

An estimated 0.4% of laryngeal cancers in Great Britain are linked to occupational asbestos exposure.[2] Laryngeal cancer risk is 38% higher in people with high levels of occupational asbestos exposure, compared with unexposed people, a meta-analysis of case-control studies showed.[2]

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Formaldehyde is classified by the International Agency for Research on Cancer (IARC) as a cause of nasopharyngeal cancer.[1] Less than 1% of nasopharyngeal cancers in Great Britain are linked to occupational exposure to formaldehyde.[2]

Nasopharyngeal cancer death risk may not be associated with formaldehyde exposure, cohort studies have shown;[3,4] however evidence is mixed.[5]

References

  1. International Agency for Research on Cancer. List of Classifications by cancer sites with sufficient or limited evidence in humans, Volumes 1 to 117*. Accessed January 2017.
  2. Slack R, Young C, Rushton L. British Occupational Cancer Burden Study Group.Occupational cancer in Britain. Nasopharynx and sinonasal cancers. Br J Cancer 2012;107 Suppl 1:S49-55.
  3. Siew SS, Kauppinen T, Kyyrönen P, et al. Occupational exposure to wood dust and formaldehyde and risk of nasal, nasopharyngeal, and lung cancer among Finnish men. Cancer Manag Res 2012;4:223-32.
  4. Coggon D, Ntani G, Harris EC, Palmer KT. Upper airway cancer, myeloid leukemia, and other cancers in a cohort of British chemical workers exposed to formaldehyde. Am J Epidemiol 2014;179(11):1301-11.
  5. Hauptmann M, Lubin JH, Stewart PA, et al. Mortality from solid cancers among workers in formaldehyde industries. Am J Epidemiol 2004;159(12):1117-30.
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Wood dust is classified by the International Agency for Research on Cancer (IARC) as a cause of nasopharyngeal cancer.[1] An estimated 10% of nasopharyngeal cancers in men in Great Britain, and around 2% in women, are linked to occupational exposure to wood dust.[2]

Nasopharyngeal cancer death risk may be 2.4 times higher in furniture and plywood workers, a pooled analysis showed;[3] however evidence is mixed.[4]

References

  1. International Agency for Research on Cancer. List of Classifications by cancer sites with sufficient or limited evidence in humans, Volumes 1 to 117*. Accessed January 2017.
  2. Slack R, Young C, Rushton L, British Occupational Cancer Burden Study Group.Occupational cancer in Britain. Nasopharynx and sinonasal cancers. Br J Cancer 2012;107 Suppl 1:S49-55.
  3. Demers PA, Boffetta P, Kogevinas M, et al. Pooled reanalysis of cancer mortality among five cohorts of workers in wood-related industries. Scand J Work Environ Health 1995;21(3):179-90.
  4. Siew SS, Kauppinen T, Kyyrönen P, et al. Occupational exposure to wood dust and formaldehyde and risk of nasal, nasopharyngeal, and lung cancer among Finnish men. Cancer Manag Res 2012;4:223-32.
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Working in rubber production is classified by IARC as probable causes of laryngeal cancer, based on limited evidence.[1]

An estimated 0.1% of laryngeal cancers in Great Britain are linked to working in the rubber production industry.[2] Laryngeal cancer risk may be 39% higher in rubber industry workers compared with the general population, a meta-analysis showed.[3]

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Exposure to printing processes (which may entail exposure to polycyclic aromatic hydrocarbons and mineral oils) is classified by IARC as probable causes of pharynx cancer, based on limited evidence.[1] Working in rubber production and sulphur mustard (mustard gas) are classified by IARC as probable causes of laryngeal cancer, based on limited evidence.[1]

Oral and pharyngeal cancer risk is 14% higher in people exposed to polycyclic aromatic hydrocarbons.[2]

Laryngeal cancer risk may be higher in people occupationally exposed to polycyclic aromatic hydrocarbons, engine exhaust, textile dust, or silica dust, and hairdressers, meta-analyses have shown.[3-7]

References

  1. International Agency for Research on Cancer. List of Classifications by cancer sites with sufficient or limited evidence in humans, Volumes 1 to 117*. Accessed January 2017. 
  2. Paget-Bailly S, Cyr D, Luce D. Occupational exposures to asbestos, polycyclic aromatic hydrocarbons and solvents, and cancers of the oral cavity and pharynx: a quantitative literature review. Int Arch Occup Environ Health 2012;85(4):341-51.
  3. Paget-Bailly S, Cyr D, Luce D. Occupational exposures and cancer of the larynx-systematic review and meta-analysis. J Occup Environ Med 2012;54(1):71-84.
  4. Chen M, Tse LA. Laryngeal cancer and silica dust exposure: a systematic review and meta-analysis. Am J Ind Med 2012;55(8):669-76.
  5. Takkouche B, Regueira-Méndez C, Montes-Martínez A. Risk of cancer among hairdressers and related workers: a meta-analysis. Int J Epidemiol 2009;38(6):1512-31.
  6. Bayer O, Cámara R, Zeissig SR, et al. Occupation and cancer of the larynx: a systematic review and meta-analysis. Eur Arch Otorhinolaryngol 2014. [Epub ahead of print]
  7. Wagner M, Bolm-Audorff U, Hegewald J, et al. Oupational polycyclic aromatic hydrocarbon exposure and risk of larynx cancer: a systematic review and meta-analysis. Occup Environ Med 2015;72(3):226-233.
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Salted fish (Chinese-style) is classified by the International Agency for Research on Cancer (IARC) as a cause of nasopharyngeal cancer; nitrosamine levels are higher in Chinese-style than other types of salted fish.[1

Nasopharyngeal cancer risk in adulthood is 2.5 times higher in people with the highest intakes of Chinese-style salted fish during childhood, versus those with the lowest, a case-control study showed.[2] Confounding by tobacco use and vegetable intake is possible.[3]

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Laryngeal cancer risk is 36% higher among people with the highest processed meat intake versus those with the lowest, a pooled analysis of case-control studies showed.[1] Laryngeal cancer risk is not associated with red or white meat intake.[1] Laryngeal cancer risk may vary with type of processed meat, a case-control study indicates.[2] Laryngeal cancer risk is higher in people with the highest fat intake versus those with the lowest, a pooled analysis of case-control studies showed.[3]

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Drinking hot maté (a traditional South American drink) is classified by the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) as a possible cause of mouth, pharyngeal and laryngeal cancers, based on limited-suggestive evidence.[1]

Oral and oropharyngeal cancer risk is around twice higher in maté drinkers versus non- or low-drinkers, a meta-analysis of case-control studies from Latin America showed.[2] This may reflect the hot temperature of the drink, or carcinogenic substances in the drink.[2]

Laryngeal cancer risk may only be associated with drinking maté in large amounts,[3,4] and/or at high temperatures,[4] case-control studies have shown.

References

  1. World Cancer Research Fund / American Institute for Cancer Research. Continuous Update Project Findings & Reports. Accessed January 2017.
  2. Dasanayake AP, Silverman AJ, Warnakulasuriya S. Maté drinking and oral and oro-pharyngeal cancer: a systematic review and meta-analysis. Oral Oncol 2010;46(2):82-6.
  3. Goldenberg D, Golz A, Joachims HZ. The beverage maté: a risk factor for cancer of the head and neck. Head Neck 2003;25(7):595-601.
  4. Stefani ED, Moore M, Aune D, et al. Maté consumption and risk of cancer: a multi-site case-control study in Uruguay. Asian Pac J Cancer Prev 2011;12(4):1089-93.
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Non-starchy vegetables and fruits (not salted or pickled), and foods containing carotenoids, are classified by the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) as probably protective against mouth, pharynx and larynx cancers, based on limited evidence.[1] An estimated 56% of oral cavity and pharynx cancers, and 45% of laryngeal cancers in the UK are linked to eating fewer than five portions of fruit and vegetables per day.[2]

Head and neck cancer (definitions vary between studies) risk is lower in people with the highest intake of the following foods, versus those with the lowest intake, meta- and pooled analyses or systematic reviews have shown:

  • Fruit – 48% lower risk (though some evidence of no association with laryngeal cancer [3,4]).[5]
  • 34% lower risk (though some evidence of no association with laryngeal cancer [3,4]).[5]
  • Vitamin C supplements – 24% lower risk in ever- versus never-users.[6]
  • Calcium supplements – 36% lower risk in ever- versus never-users.[6]
  • Caffeinated coffee – 39% lower risk in 4 cups/day versus non-drinkers.[7]
  • Green tea – 20% lower risk.[8]
  • Folate (natural, fortification or supplements) – 35% lower risk.[9]

References

  1. World Cancer Research Fund / American Institute for Cancer Research. Continuous Update Project Findings & Reports. Accessed January 2017.
  2. Parkin DM, Boyd L. Cancers attributable to dietary factors in the UK in 2010. I Low consumption of fruit and vegetables. Br J Cancer 2011; 105 (S2):S19-S23.
  3. Maasland DH, van den Brandt PA, Kremer B, et al. Consumption of vegetables and fruits and risk of subtypes of head-neck cancer in the Netherlands Cohort Study. Int J Cancer 2014.
  4. Freedman ND, Park Y, Subar AF, et al. Fruit and vegetable intake and head and neck cancer risk in a large United States prospective cohort study. Int J Cancer 2008;122(10):2330-6.
  5. Chuang SC, Jenab M, Heck JE, et al. Diet and the risk of head and neck cancer: a pooled analysis in the INHANCE consortium. Cancer Causes Control 2012;23(1):69-88.
  6. Li Q, Chuang SC, Eluf-Neto J, et al. Vitamin or mineral supplement intake and the risk of head and neck cancer: pooled analysis in the INHANCE consortium. Int J Cancer 2012;131(7):1686-99.
  7. Galeone C, Tavani A, Pelucchi C, et al. Coffee and tea intake and risk of head and neck cancer: pooled analysis in the international head and neck cancer epidemiology consortium. Cancer Epidemiol Biomarkers Prev 2010;19(7):1723-36.
  8. Wang W, Yang Y, Zhang W, et al. Association of tea consumption and the risk of oral cancer: A meta-analysis. Oral Oncol 2014;50(4):276-81.
  9. Galeone C, Edefonti V, Parpinel M, et al. Folate intake and the risk of oral cavity and pharyngeal cancer: A pooled analysis within the International Head and Neck Cancer Epidemiology Consortium. Int J Cancer 2015;136(4):904-14.
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Oral cancer risk is 26-47% lower in people who do moderate/high levels of recreational physical activity, versus those who do very little/no recreational physical activity, a pooled analysis showed.[1] Pharyngeal cancer risk is 33-42% lower in people with moderate/high physical activity levels, versus very low/no physical activity.[1] The association may be stronger in males, younger people, ever-smokers and ever-drinkers.[1]

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Laryngeal cancer risk is lower in people who are overweight or obese (body mass index [BMI] 25+) compared with those who are a healthy weight (BMI 18.5-25), a pooled analysis of case-control studies showed; however this may be limited to tobacco or alcohol users, and reverse causality (weight loss caused by early symptoms of cancer) is possible.[1] Laryngeal cancer risk is lower in people with lower levels of recreational physical activity, a pooled analysis of case-control studies showed.[2]

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Head and neck cancer (definitions vary between studies) risk is lower in people who use the following medications or have the following medical conditions, meta- and pooled analyses, systematic reviews or cohort studies have shown:

  • Allergic rhinitis – 47% reduced risk of head and neck cancer (HNC) (men only, confounding by tobacco use is possible).[1]
  • Aspirin – 25% reduced risk of HNC for long-term use for 5 years or more, versus non-use.[2]
  • Parkinson’s disease – 21% reduced risk of laryngeal cancer (men only, confounding by tobacco use is possible).[3]
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The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) make no judgement on the association between mouth, pharynx and larynx cancer risk and intake of cereals (grains) and their products; starchy roots, tubers, and plantains; dietary fibre; pulses (legumes); meat; poultry; fish; eggs; milk and dairy products; total fat; animal fats; plant oils; coffee; tea; frying; grilling (broiling) and barbecuing (charbroiling); protein; vitamin A; retinol; thiamin; riboflavin; niacin; folate; vitamin C; vitamin E; calcium; iron; selenium; body fatness; or energy intake, due to limited evidence.[1]

Head and neck cancer (definitions vary between studies) risk is not associated with the following factors, meta- and pooled analyses or systematic reviews have shown:

  • Overweight and obesity[2] (lower risk in overweight and obese people is probably due to residual confounding by smoking[3-6]).
  • Meat (except 91% higher risk with highest versus lowest processed meat consumption).[7]
  • Black tea.[8,9]
  • Vitamin D blood levels.[10]
  • Diabetes (though some evidence of risk increase in never-smokers).[11]
  • Non-aspirin non-steroidal anti-inflammatory drugs (NSAIDs).[12]
  • Systemic lupus erythematosus (oropharyngeal cancer).[13]
  • Marijuana smoking.[14-16]
  • Vitamin or mineral supplement use.[17]
  • Diabetes (though some evidence of higher risk in never-smokers).[11]
  • Coffee.[18]
  • Sweetened carbonated drinks.[19]

References

  1. World Cancer Research Fund / American Institute for Cancer Research. Continuous Update Project Findings & Reports. Accessed January 2017.
  2. Gaudet MM, Patel AV, Sun J, et al. Prospective studies of body mass index with head and neck cancer incidence and mortality. Cancer Epidemiol Biomarkers Prev 2012;21(3):497-503.
  3. Gaudet MM, Olshan AF, Chuang SC, et al. Body mass index and risk of head and neck cancer in a pooled analysis of case-control studies in the International Head and Neck Cancer Epidemiology (INHANCE) Consortium. Int J Epidemiol 2010;39(4):1091-102.
  4. Bhaskaran K, Douglas I, Forbes H, et al. Body-mass index and risk of 22 specific cancers: a population-based cohort study of 524 million UK adults. Lancet 2014 Aug;384(9945):755-65.
  5. Etemadi A, O'Doherty MG, Freedman ND, et al. A prospective cohort study of body size and risk of head and neck cancers in the NIH-AARP diet and health study. Cancer Epidemiol Biomarkers Prev 2014;23(11):2422-9.
  6. Maasland DH, van den Brandt PA, Kremer B, et al. Body mass index and risk of subtypes of head-neck cancer: the Netherlands Cohort Study. Sci Rep. 2015 Dec 4;5:17744.
  7. Xu J, Yang XX, Wu YG, Li XY, Bai B. Meat consumption and risk of oral cavity and oropharynx cancer: a meta-analysis of observational studies. PLoS One 2014 15;9(4):e95048.
  8. Galeone C, Tavani A, Pelucchi C, et al. Coffee and tea intake and risk of head and neck cancer: pooled analysis in the international head and neck cancer epidemiology consortium. Cancer Epidemiol Biomarkers Prev 2010;19(7):1723-36.
  9. Wang W, Yang Y, Zhang W, et al. Association of tea consumption and the risk of oral cancer: A meta-analysis. Oral Oncol 2014;50(4):276-81.
  10. Skaaby T, Husemoen LL, Thuesen BH, et al. Prospective population-based study of the association between serum 25-hydroxyvitamin-D levels and the incidence of specific types of cancer. Cancer Epidemiol Biomarkers Prev 2014;23(7):1220-9.
  11. Stott-Miller M, Chen C, Chuang SC, et al. History of diabetes and risk of head and neck cancer: a pooled analysis from the international head and neck cancer epidemiology consortium. Cancer Epidemiol Biomarkers Prev 2012;21(2):294-304.
  12. Tang L, Hu H, Liu H, et al. Association of nonsteroidal anti-inflammatory drugs and aspirin use and the risk of head and neck cancers: a meta-analysis of observational studies. Oncotarget. 2016 Aug 12. doi: 10.18632/oncotarget.
  13. Cao L, Tong H, Xu G, et al. Systemic lupus erythematous and malignancy risk: a meta-analysis. PLoS One. 2015 Apr 17;10(4):e0122964.
  14. Berthiller J, Lee YC, Boffetta P, et al. Marijuana smoking and the risk of head and neck cancer: pooled analysis in the INHANCE consortium. Cancer EpidemiolBiomarkers Prev 2009;18(5):1544-51.
  15. 1Marks MA, Chaturvedi AK, Kelsey K, et al. Association of marijuana smoking with oropharyngeal and oral tongue cancers: pooled analysis from the INHANCE consortium. Cancer Epidemiol Biomarkers Prev 2014;23(1):160-71.
  16. de Carvalho MF, Dourado MR, Fernandes IB, et al. Head and neck cancer among marijuana users: a meta-analysis of matched case-control studies. Arch Oral Biol. 2015;60(12):1750-5.
  17. Li Q, Chuang SC, Eluf-Neto J, et al. Vitamin or mineral supplement intake and the risk of head and neck cancer: pooled analysis in the INHANCE consortium. Int J Cancer 2012;131(7):1686-99.
  18. Turati F, Galeone C, La Vecchia C, et al. Coffee and cancers of the upper digestive and respiratory tracts: meta-analyses of observational studies. Ann Oncol 2011;22(3):536-44.
  19. Boyle P, Koechlin A, Autier P. Sweetened carbonated beverage consumption and cancer risk: meta-analysis and review. Eur J Cancer Prev. 2014 Sep;23(5):481-90.
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Acknowledgements

We are grateful to the many organisations across the UK which collect, analyse, and share the data which we use, and to the patients and public who consent for their data to be used. Find out more about the sources which are essential for our statistics.

Cancer stats explained

See information and explanations on terminology used for statistics and reporting of cancer, and the methods used to calculate some of our statistics.

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