Current evidence indicates that approximately one-third of cancer deaths in Australia can be attributed to known and avoidable risk factors. Appropriate prevention strategies have the potential to reduce cancer incidence.
Risk Factors:
The key modifiable risk factors for cancer are defined as the SNAPSS risk factors. These are:
- Smoking/exposure to tobacco smoke
- Nutrition (concerns about poor diet/nutrition)
- Alcohol (risky alcohol consumption)
- Physical activity (inadequate exercise or being overweight)
- Sun exposure (exposure to harmful ultraviolet radiation)
- Stress.
Prevention Strategies:
Prevention and early detection strategies include: (Ref : 2)
- promotion of healthy lifestyles (stopping smoking, healthy diet, healthy weight, limiting alcohol intake)
- reducing risky behaviours (stopping smoking, ‘sun smart’ behaviours).
MAJOR RISK FACTORS FOR HEAD AND NECK CANCER
Tobacco smoking and alcohol are major risk factors for head and neck cancer.
Known risk factors for head and neck squamous cell cancer include:
- tobacco smoking (cigarettes, pipes and cigars)
- excessive consumption of alcohol
- viral infections, including human papilloma virus (HPV16) seropositivity for cancers of lingual and palatine tonsils
- pre-existing oral lesions
- ultraviolet radiation for lip cancer
- age
- male gender
A. Tobacco smoking and alcohol consumption
Tobacco smoking is associated with a ten-fold increase in risk of head and neck cancer, while a daily
intake of 100g alcohol is associated with a six-fold increase. (Ref : 3) Tobacco and alcohol have a synergistic effect on risk of head and neck cancer.
It is important that anyone with lifestyle risk factors associated with head and neck cancer who presents with symptoms suggestive of a cancer of the head and neck is referred for appropriate investigation.
B. Human Papilloma Virus
The Human Papilloma virus (HPV) has been identified as an etiological agent for head and neck cancers – that is, HPV has been associated with the development of certain types of head and neck cancers. (Ref : 4) Approximately 35% of oral cancers are positive for HPV DNA, and 90–95% are positive for HPV-16. (Ref : 5) These cases tend to occur in younger men who do not smoke or drink alcohol, and have a favourable outcome.
Studies suggest an association between HPV-positive head and neck cancers and sexual behaviour, including increasing numbers of both vaginal and oral sex partners, and a history of genital warts. There is also a correlation between marijuana use and the risk of developing an HPV-16-positive head and neck cancer. (Ref : 6)
Research into transmission of oral and oropharyngeal HPV is only in early stages, and opportunities for risk reduction are not yet clear. An absence of clinically identifiable premalignant lesions means that screening is dependent on molecular biomarkers.
C. Pre-existing oral lesions
Pre-existing oral disease, such as leukoplakia, lichen planus, erythroplakia and submucosal fibrosis, have an increased risk of progressing to malignancy. Oral leukoplakia is the most common form of premalignant oral lesion, however several studies have found that only a small number of leukoplakias eventually progress to malignancy. (Ref : 7)
Oral patches with suspicious features, such as bleeding, should be referred promptly for appropriate assessment and biopsy by a head and neck cancer specialist. Many health professionals will offer treatment and surveillance within a multidisciplinary clinic.
D. Age and gender
About 90% of oral cancers occur in people in people older than 50 years of age. The incidence of oral cancers is also about two-thirds higher amongst men than women. (Ref : 8)
E. Aboriginal and Torres Strait Islander status
The incidence of oral cancer is about three times higher among Australians from Aboriginal and Torres Strait Islander communities compared with non-Indigenous Australians. (Ref : 9)
Identifying people who may be at higher risk of head and neck cancer enables the GP or other health professionals to develop a surveillance plan and/or monitor for symptoms that may require further investigation.
Tailored interventions are also required to reach and educate high risk groups because they generally constitute socially disadvantaged groups. (Ref : 9)
References:
1. Cancer Council Australia. National Cancer Prevention Policy 2007–2009.
2. Royal Australasian College of General Practitioners. Putting prevention into practice (the Green Book) 2nd Edition RACGP Melbourne 2006
3. Blot WJ et al Smoking and Drinking in relation to oral and Pharyngeal Cancer Cancer Res 1988 Jun 1;48(11):3282-7
4. Gillison Ml, 2007 Current topics in the epidemiology of oral cavity and oropharyngeal cancers, Head and Neck29:779-992
5. D’Souza G et al , 2007, Case Control study of human papillomavirus and oropharyngeal cancer. N
Eng J Med 2007:356(19):1944-56
6. Gillison ML et al, 2010Distinct risk factor profiles for human papillomavirus type 16 positive and
human papillomavirus type 16 negative head and neck cancers Cancer causes and Control. 2010:21(9):1369-1378
7. Reibel J, 2003, Prognosis of oral pre-malignant lesions; significance of clinical, histopathological and molecular biological characteristics, Crit Rev Oral Biol 2003:14:47-62
8. Cottrell J et al 2007, Comparing cancer profiles and survival of aboriginal and non-aboriginal patients in South Australia; where are the opportunities for improving Aboriginal health? Asian 8:495-501
9. Victorian Department of Human Services. Patient management framework Head and neck tumour
stream: larynx, pharynx and oral cancer, a guide to consistent cancer care. Metropolitan Health and
Aged Care Services Division. Melbourne Victoria 2006
10. South Australian Head and Neck Cancer Pathway Sep 2013