Cervical Cancer Risk Factors

This page presents risk factors for cervical cancer including, human papillomavirus, smoking, socioeconomic status and other factors.

Cervical cancer risk factors:

 
 

Human papillomavirus (HPV) and cervical cancer risk

Members of the HPV family have been detected in cervical tumours worldwide with studies showing the presence of HPV in virtually all cervical tumours tested 1.

The highest risks are associated with HPV types 16 and 18. Most HPV infections will not progress to cervical intraepithelial neoplasia (CIN) . However, it is believed that cervical cancer will not develop without the presence of persistent HPV DNA and it has been proposed as the first ever identified “necessary cause” of a human cancer 2.

Genital HPV is generally sexually transmitted through contact with infected cervical, vaginal, vulvar, penile or anal epithelium. Genital HPV infection may involve areas that are not easily covered by a condom so correct condom use may not protect against infection.

An analysis of studies on the prevalence of HPV infection in the population led to the conclusions that HPV is more common in younger women than older women, that HPV is rarely detected in women with no previous sexual activity and that there are no apparent geographical differences in HPV prevalence.

The percentage of the study populations who were HPV positive varied from 0% to 48% depending on the group studied. Results also show that HPV 16 infection is more common than any other classified type of HPV 3. Risk factors for HPV infection include number of sexual partners, a relatively recent new sexual relationship and a history of previous miscarriage 4.

A study has shown that the main risk factors for CIN 3 among HPV positive women are early age at first intercourse, long duration of the most recent sexual relationship and cigarette smoking. 4

For cigarette smoking there is a strong dose-response relationship. The risk of CIN 3 for women who were HPV positive and smoking 20 or more cigarettes a day was two and a half times that of women who had never smoked. The authors concluded that even though smoking was not a risk factor for HPV, smoking acted with HPV to cause cervical neoplasia (see also Smoking section below).

Suggested co-factors for cervical cancer include age at first intercourse, number of life-time partners, co-infection with herpes simplex virus-2 or chlamydia trachomatis, parity, age at first birth, oral contraceptive use and family history 5,9,25-28. A lower risk has been shown in partners of men who have been circumcised. 29

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Smoking and cervical cancer risk

Cigarette smoking has been linked to inactivation in cervical tumours of the fragile histidine triad 6 putative tumour suppressor gene (which is also altered in most tobacco-associated lung cancers).

Smoking may also be associated with a decrease in the number of Langerhans’ immune cells in the cervix epithelium, suggesting a decrease in epithelial cell-mediated immune responses in smokers 7, 8.

A meta-analysis showed that risk of squamous cell cervical cancer was increased by almost 50% in current smokers, although there was no risk increase for adenocarcinomas. 9

Reduction in early cervical lesion size in women who gave up smoking after diagnosis has been reported 10. Also smokers have been found to have a 3-fold increased risk of treatment failure of CIN compared to non-smokers and therefore require more intensive follow-up after treatment 11.

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Socio-economic status and cervical cancer risk

In England and Wales 12, incidence and mortality from cervical cancer has been analysed by to Carstairs deprivation category ( Figure 4.1).

Figure 4.1: European age-standardised incidence of and mortality,cervical cancer by deprivation category, England and Wales, 1990-93

Download this chart (27KB)

Women living in the most deprived areas have rates more than three times as high as those in the least deprived areas. A strong positive association between cervical cancer and deprivation has also been described for incidence data from Scotland 13.

In addition a link has been demonstrated between social class and cervical cancer. Data from a longitudinal study, representing 1% of the England and Wales population, indicates that cervical cancer incidence is considerably higher among women of working age in manual than in non-manual classes 14.

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Other cervical cancer risk factors

As with smoking, the association between oral contraceptive (OC) use and cervical cancer is complicated by possible confounding with sexual behaviour 15. A meta-analysis 9 found risk of both types of cervical cancer was doubled in women using OCs for 10 or more years. There were smaller risk increases for shorter durations of use.

The risk increase is temporary and returns to the level of non-users after 10 years. 17

Other studies 20, 21 have investigated the use of hormone replacement therapy and cervical cancer, but there are no clear conclusions.

A recent meta-analysis showed that women with HIV/AIDS have a six-fold increased risk of cervical cancer and women who have undergone organ transplant have more than double the risk, strongly suggesting that immunosuppression plays a role. 22

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References for cervical cancer risk factors

  1.  Walboomers, J.M.M. and C. Meijer, Do HPV-negative cervical carcinomas exist?[editorial]. Journal Pathology, 1997. 181: p. 253-254.
  2.  Bosch, F.X., et al., The causal relation between human papillomavirus and cervical cancer. Journal of clinical pathology, 2002. 55(4): p. 244-265.
  3.  International Agency for Research on Cancer, IARC Monographs on the evaluation of carcinogenic risks to humans: human papillomaviruses. Vol. 64. 1995, Lyon: World Health Organisation.
  4.  Deacon, J., et al., Sexual behaviour and smoking as determinants of cervical HPV infection and of CIN 3 among those infected. A case-control study nested within the Manchester cohort. British Journal of Cancer, 2000. 83: p. 1565-1572.
  5.  Schottenfeld, D. and J. Fraumeni, eds. Cancer epidemiology and prevention. 2nd ed. 1996, Oxford University Press: Oxford.
  6.  Holschneider, C., et al. Lost fragile histidine triad (FHIT) gene expression may link cigarette smoking and cervical cancer [abstract]. in Program and Abstracts of the Society for Gynecologic Oncologists 31st Annual Meeting; February 5-9. 2000. San Diego, California.
  7.  Derchain, S., et al., Langerhans' cells in cervical condyloma and intraepithelial neoplasia in smoking and non-smoking adolescents. Acta Derm Venereol, 1996. 76(6): p. 493-494.
  8.  Poppe, W., et al., Langerhans' cells and L1 antigen expression in normal and abnormal squamous epithelium of the cervical transformation zone. Gynecol Obstet Invest, 1996. 41(3): p. 207-213.
  9.  Berrington de Gonzalez, A., et al., Comparison of risk factors for squamous cell and adenocarcinomas of the cervix: a meta-analysis. Br J Cancer, 2004. 90(9): p. 1787-91.
  10.  Szarewski, A., M.J. Jarvis, and P. Sasieni, Effect of smoking cessation on cervical lesion size. Lancet, 1996. 347: p. 941-943.
  11.  Acladious, N., et al., Persistent human papillomavirus infection and smoking increase risk of failure of treatment of cervical intraepithelial neoplasia (CIN). International Journal of Cancer, 2002. 98(3): p. 435-439.
  12.  Quinn, M., et al., Cancer Trends in England & Wales 1950-1999. Vol. SMPS No. 66. 2001: TSO.
  13.  Harris, V., et al., Cancer Registration Statistics: Scotland 1986-1995. 1998, Edinburgh: ISD Scotland Publications.
  14.  Brown, J., S. Harding, and A. Bethune, Incidence of Health of the nation cancers by social class. Population Trends, 1997.
  15. .
  16.  Zondervan, K., et al., Oral Contraceptives and Cervical Cancer- Further findings from the Oxford Family Planning Association contraceptive study. British Journal of Cancer, 1996. 73: p. 1291-1297.
  17.  Beral, V., C. Hermon, and C. Kay, Mortality associated with oral contraceptive use: 25 year follow up of cohort of 46 000 women from Royal College of General practitioners' oral contraception study. British Medical Journal, 1999. 318: p. 96-100.
  18.  Appleby, P., et al., Cervical cancer and hormonal contraceptives: collaborative reanalysis of individual data for 16,573 women with cervical cancer and 35,509 women without cervical cancer from 24 epidemiological studies. Lancet, 2007. 370 (9599): p. 1609-21.
  19.  Hildesheim, A., et al., HPV co-factors related to the development of cervical cancer: results from a population-based study in Costa Rica. British Journal of Cancer, 2001. 84(9): p. 1219-1226.
  20.  Munoz, N., et al., Role of parity and human papillomavirus in cervical cancer: the IARC multicentric case-control study. Lancet, 2002. 359: p. 1093-1101.
  21.  Parazzini, F., et al., Case-control study of ostrogen replacement therapy and risk of cervical cancer. British Medical Journal, 1997. 315: p. 85-88.
  22.  Lacey, J.J., et al., Use of hormone replacement therapy and adenocarcinomas and squamous cell carcinomas of the uterine cervix. Gynecologic Oncology, 2000. 77: p. 149-154.
  23.  Grulich, A.E., et al., Incidence of cancers in people with HIV/AIDS compared with immunosuppressed transplant recipients: a meta-analysis.Lancet, 2007. 370(9581): p. 59-67.
  24.  Gallagher, B., et al., Cancer incidence in New York State acquired immunodeficiency syndrome patients.American Journal of Epidemiology, 2001. 154(6): p. 544-556.
  25.  Dal Maso, L., Serraino, D. and Franceschi, S. Epidemiology of AIDS-related tumours in developed and developing countries. European Journal of Cancer, 2001. 37(10): p. 1188-1201.
  26.  Smith, J.S., et al., Herpes Simplex Virus-2 as a Human Papillomavirus Cofactor in the Etiology of Invasive Cervical Cancer. JNCI, 2002. 94(21): p. 1604-1625.
  27.  Smith, J.S., et al., Chlamydia trachomatis and invasive cervical cancer: a pooled analysis of the IARC multicentric case-control study. Int J Cancer, 2004. 111(3): p. 431-9.
  28.  Madeleine, M.M., et al., Risk of cervical cancer associated with Chlamydia trachomatis antibodies by histology, HPV type and HPV cofactors. Int J Cancer, 2007. 120(3): p. 650-5.
  29.  Hemminki, K., et al., Familial risks for cervical tumors in full and half siblings: etiologic apportioning. Cancer Epidemiol Biomarkers Prev, 2006. 15(7): p. 1413-4.
  30.  Castellsague, X., et al., Male circumcision, penile human papillomavirus infection, and cervical cancer in female partners. N Engl J Med, 2002. 346(15): p. 1105-1112.