Cervical cancer risk factors

Preventable cases

Cervical cancer cases are preventable, UK, 2015

 

Caused by infections

Cervical cancer cases caused by infections, UK, 2015

 

 

Caused by smoking

Cervical cancer cases caused by smoking, UK, 2015

 

Caused by occupation

Cervical cancer cases caused by workplace exposures, UK, 2015

 

International Agency for Research on Cancer (IARC) classifies the role of this risk factor in cancer development.[1] An estimated 10% of cervical cancers in the UK are linked to use of OCs.[2]

Cervical cancer risk is up to doubled in current OC users who have used OCs for 5+ years, compared with never users, pooled- and meta-analyses have shown.[3-5] Cervical cancer risk may increase with longer duration of use,[3,4] but is no higher in women who last took OCs 10+ years ago, compared with never-users.[3]

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Having children

Cervical cancer risk is 15% higher in women who have had 1 full-term pregnancy compared with those who have had none, a pooled analysis showed; the risk increases with number of full-term pregnancies.[1] Cervical cancer risk among parous women is 64% higher in those with 7+ full-term pregnancies, versus those with 1 or 2, this pooled analysis showed.[1] The association with parity is limited to squamous cell carcinoma, with no association for adenocarcinoma, this pooled analysis showed.[1] The reasons for these associations are unknown.

Younger age at first giving birth

Cervical cancer risk among parous women is 77% higher in those under 17 years old at their first full-term pregnancy, compared with those aged 25 or older, a pooled analysis has shown; the risk decreases with older age at first full-term pregnancy.[1] The association with age at first full-term pregnancy is limited to squamous cell carcinoma, with no association for adenocarcinoma, this pooled analysis showed.[1]

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Cervical cancer risk among parous women is 77% higher in those under 17 years old at their first full-term pregnancy, compared with those aged 25 or older, a pooled analysis has shown; the risk decreases with older age at first full-term pregnancy.[1] The association with age at first full-term pregnancy is limited to squamous cell carcinoma, with no association for adenocarcinoma, this pooled analysis showed.[1]

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International Agency for Research on Cancer (IARC) classifies the role of this risk factor in cancer development.[1] 21% of cervical cancer cases in the UK are caused by smoking.[2]

Cervical squamous cell carcinoma (SCC) risk is 46% higher in current smokers versus never-smokers, a pooled analysis showed.[3] Cervical SCC (invasive or in situ) risk increases with number of cigarettes smoked per day, a pooled analysis showed.[3]

Cervical SCC risk is not associated with past smoking, only current smoking, a pooled analysis showed.[3] Carcinoma in situ risk is 83% higher in current smokers, and 32% higher in past smokers, versus never-smokers, a pooled analysis showed.[3] Cervical adenocarcinoma risk is not associated with smoking, a pooled analysis showed.[3] Cervical cancer risk may be higher in current smokers because they are more likely to have human papillomavirus (HPV) infection (more likely to contract HPV, less able to clear HPV, or both),[4] or because smoking causes cancerous progression in HPV-infected cells.[3]

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Cervical cancer risk is 73% higher in never-smoking women exposed to environmental tobacco smoke, compared with those who are not exposed, a meta-analysis showed.[1]

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Tetrachloroethylene is classified by the International Agency for Research on Cancer (IARC) as a cause of cervical cancer, based on limited evidence.[1] An estimated 0.7% of cervical cancers in the UK are linked to tetrachloroethylene exposure.[2]

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Cervical squamous cell carcinoma risk is 74-80% higher in women with a first-degree relative (mother, sister, daughter) with cervical squamous cell carcinoma, compared with the general population, a cohort study showed.[1] Cervical adenocarcinoma risk is 39-69% higher in women with a first-degree relative with cervical squamous cell carcinoma, compared with the general population, a cohort study showed.[1]

This probably reflects shared environmental risk factors including human papillomavirus (HPV) infection, as well as possible genetic factors.[1]

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Diethylstilboestrol (DES) exposure in utero is classified by the International Agency for Research on Cancer (IARC) as a cause of cervical adenocarcinoma; it is classified as a probable cause of cervical squamous cell carcinoma, based on limited evidence.[1]

Cervical cancer and high-grade carcinoma in situ risk is 2.3 times higher in women who were exposed in utero to DES, a cohort study showed.[2]

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Cervical dysplasia risk is higher in women with systemic lupus erythematosus, a meta-analysis and cohort study have shown;[1,2] though there is some evidence of no association between cervical cancer and systemic lupus erythematosus.[3] Cervical cancer risk may be higher in women with inflammatory bowel disease, cohort studies have shown;[4,5] though this may be limited to high-dose use of the immunosuppressant drug azathioprine.[5]

Use of immunosuppressant drugs in autoimmune conditions may inhibit human papillomavirus (HPV) clearance.

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Carrots are classified by The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) as possibly protective against cervical cancer, based on limited-suggestive evidence.[1]

Cervical cancer risk is 40-49% lower in women with the highest dietary vitamin A, carotene and other carotenoids intake versus those with the lowest, a meta-analysis showed.[2] Carotenoids are found at high levels in carrots; some are precursors of vitamin A but also have independent antioxidant properties.

Cervical cancer risk is 45% lower in women who have ever used an intrauterine device (IUD) Open a glossary item versus never-users, a meta-analysis showed; IUD use may reduce risk of HPV progression to cervical cancer.[3]

References

  1. World Cancer Research Fund / American Institute for Cancer Research. Continuous Update Project Findings & Reports. Accessed January 2017.
  2. Zhang X, Dai B, Zhang B, Wang Z. Vitamin A and risk of cervical cancer: a meta-analysis. Gynecol Oncol 2012;124(2):366-73.
  3. Castellsagué X, Díaz M, Vaccarella S, et al. Intrauterine device use, cervical infection with human papillomavirus, and risk of cervical cancer: a pooled analysis of 26 epidemiological studies. Lancet Oncol 2011;12(11):1023-31.
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The World Cancer Research Fund / American Institute for Cancer Research (WCRF/AICR) make no judgement on the association between cervical cancer risk and intake of non-starchy vegetables; fruits; milk; retinol; vitamin E; alcohol; body fatness; and adult attained height, due to limited evidence.[1]

Cervical cancer risk is not associated with the following factors, meta- and pooled analyses or systematic reviews have shown:

  • Physical activity[2] (though some evidence of risk decrease[3]).
  • Overweight and obesity (though some evidence of risk increase,[4] perhaps due to lower cervical screening attendance in larger women[5]).
  • Postmenopausal hormone replacement therapy.[6]
  • Organ transplant receipt[7,8] (some evidence of risk increase, this variation may reflect differing use of cervical screening in the transplant population over time/between countries[9,10]).
  • Non-steroidal anti-inflammatory drugs (NSAIDs) use[11] (also no effect on risk of progression from carcinoma in situ to cancer[12]).
  • Statins.[13]
  • Undergoing in vitro fertilisation (IVF).[14]
  • Rheumatoid arthritis.[15]

References

  1. World Cancer Research Fund / American Institute for Cancer Research. Continuous Update Project Findings & Reports. Accessed January 2017.
  2. Cust AE. Physical activity and gynecologic cancer prevention. Recent Results Cancer Res 2011;186:159-85.
  3. Lee JK, So KA, Piyathilake CJ, Kim MK. Mild obesity, physical activity, calorie intake, and the risks of cervical intraepithelial neoplasia and cervical cancer. PLoS One 2013;8(6):e66555.
  4. Dugué PA, Rebolj M, Hallas J, et al. Risk of cervical cancer in women with autoimmune diseases, in relation with their use of immunosuppressants and screening: Population-based cohort study. Int J Cancer 2015;136(6):E711-9.
  5. Maruthur NM, Bolen SD, Brancati FL, Clark JM. The Association of Obesity and Cervical Cancer Screening: A Systematic Review and Meta-Analysis. Obesity (Silver Spring) 2009; 17(2): 375-381.
  6. Gadducci A, Barsotti C, Cosio S, Domenici L, Riccardo Genazzani A. Smoking habit, immune suppression, oral contraceptive use, and hormone replacement therapy use and cervical carcinogenesis: a review of the literature. Gynecol Endocrinol. 2011;27(8):597-604.
  7. Madeleine MM, Finch JL, Lynch CF, et al. HPV-related cancers after solid organ transplantation in the United States. Am J Transplant 2013;13(12):3202-9.
  8. Engels EA, Pfeiffer RM, Fraumeni JF Jr, et al. HPV-related cancers after solid organ transplantation in the United States. JAMA 2011;306(17):1891-901.
  9. Castellsagué X, Pawlita M, Roura E, et al. Prospective seroepidemiologic study on the role of Human Papillomavirus and other infections in cervical carcinogenesis: evidence from the EPIC cohort. Int J Cancer 2014;135(2):440-52.
  10. 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.
  11. Wilson JC, O'Rorke MA, Cooper JA, et al. Non-steroidal anti-inflammatory drug use and cervical cancer risk: a case-control study using the Clinical Practice Research Datalink. Cancer Epidemiol 2013;37(6):897-904.
  12. Grabosch SM, Shariff OM, Wulff JL, Helm CW. The Association of Obesity and Cervical Cancer Screening: A Systematic Review and Meta-Analysis. Cochrane Database Syst Rev 2014;4:CD004121.
  13. Liu Y, Qin A, Li T, Qin X, Li S. Non-steroidal anti-inflammatory agents to induce regression and prevent the progression of cervical intraepithelial neoplasia. Gynecol Oncol 2014;133(3):647-55.
  14. Li LL, Zhou J, Qian XJ, Chen YD. Meta-analysis on the possible association between in vitro fertilization and cancer risk. Int J Gynecol Cancer 2013;23(1):16-24.
  15. Simon TA, Thompson A, Gandhi KK, et al. Incidence of malignancy in adult patients with rheumatoid arthritis: a meta-analysis. Arthritis Res Ther. 2015 Aug 15;17:212.
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99.8% of cervical cancer cases in the UK are preventable.[1]

Cervical cancer is associated with a number of risk factors.[2,3]

Cervical Cancer Risk Factors

  Increases risk Decreases risk
'Sufficient' or 'convincing' evidence
  • Diethylstilbestrol (in utero exposure)[a]
  • Oestrogen-progestogen contraceptives
  • Human immunodeficiency virus (HIV) type 1
  • Human papillomavirus (HPV) types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59
  • Tobacco smoking
 
'Limited' or 'Probable' evidence
  • HPV types 26, 53, 66, 67, 68, 70, 73, 82
 

International Agency for Research on Cancer (IARC) and World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) classifications.

a IARC classifies evidence on in utero diethylstilbestrol exposure as sufficient for cervical adenocarcinoma; and as limited for cervical squamous cell carcinoma.

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International Agency for Research on Cancer (IARC) classifies the role of this risk factor in cancer development.[1]

HPV infection

99.8% of cervical cancer cases in the UK are caused by HPV infection;[2] however some HPV types are high-risk for cervical cancer, others are low-risk.

HPV infection is common, but progresses to cervical cancer in a minority of cases.[3] Around 12% of women without cervical abnormalities in the UK and Ireland are infected with high-risk HPV types, a meta-analysis has shown.[4] The highest prevalence is in younger women.[4] Around half of HPV infections clear within 6-12 months, though high-risk HPV types persist longer than low-risk types, a meta-analysis showed.[5]

Fewer than 10% of persistent HPV infections progress to carcinoma in situ,[5] which left untreated, can progress to cervical cancer.[3]

HPV16 and HPV18 account for 58% and 16% respectively of all cervical cancer cases in Europe, a pooled analysis showed.[6] These types are protected against by the UK HPV vaccination programme.

Cervical cancer risk is not associated with infection with low-risk HPV types, cohort studies have shown.[7,8] Cervical cancer risk is higher in women with genital warts (GW) versus those without, a cohort study showed;[9] though GW are usually caused by low-risk HPV types (6 and 11), co-infection with high-risk HPV types is likely.[9]

HPV exposure

Other factors may be associated with cervical cancer risk because they increase the risk of Human papillomavirus (HPV) exposure or persistent HPV infection (and/or may have direct effects, independent of HPV).[10]

Cervical cancer risk is almost three times higher in women who have had 6 or more sexual partners, compared with those who have had only one, a pooled analysis showed.[11] Cervical cancer risk is around doubled in women who first had sexual intercourse aged 14 or younger, compared with those who did so aged 25 or older, a pooled analysis showed.[11]

Cervical cancer risk is around halved in women whose only current male sexual partner is circumcised, compared with those whose partner is uncircumcised, a pooled analysis showed;[12] HPV prevalence is lower in circumcised versus uncircumcised men, a meta-analysis showed.[13]

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. Brown KF, Rumgay H, Dunlop C, et al. The fraction of cancer attributable to known risk factors in England, Wales, Scotland, Northern Ireland, and the UK overall in 2015. British Journal of Cancer 2018.
  3. Kulasingam SL, Havrilesky L, Ghebre R, Myers ER. Screening for Cervical Cancer: A Decision Analysis for the U.S. Preventive Services Task Force. Rockville (MD): Agency for Healthcare Research and Quality (US); 2011.
  4. Anderson L, O'Rorke M, Jamison J, Wilson R, Gavin A; HPV Working Group members Prevalence of human papillomavirus in women attending cervical screening in the UK and Ireland: new data from northern Ireland and a systematic review and meta-analysis. J Med Virol 2013;85(2):295-308.
  5. Rositch AF, Koshiol J, Hudgens MG. Patterns of persistent genital human papillomavirus infection among women worldwide: a literature review and meta-analysis. Int J Cancer 2013;133(6):1271-85.
  6. Smith JS, Lindsay L, Hoots, et al. Human papillomavirus type distribution in invasive cervical cancer and high-grade cervical lesions: a meta-analysis update. Int J Cancer 2007;121(3):621-32.
  7. Castle PE, Hunt WC, Langsfeld E, Wheeler CM; New Mexico HPV Pap Registry Steering Committee. Three-year risk of cervical precancer and cancer after the detection of low-risk human papillomavirus genotypes targeted by a commercial test. Obstet Gynecol 2014;123(1):49-56.
  8. Thomsen LT, Frederiksen K, Munk C, et al. High-risk and low-risk human papillomavirus and the absolute risk of cervical intraepithelial neoplasia or cancer. Obstet Gynecol 2014;123(1):57-64.
  9. Blomberg M, Friis S, Munk C, Bautz A, Kjaer SK. Genital warts and risk of cancer: a Danish study of nearly 50 000 patients with genital warts. J Infect Dis 2012;205(10):1544-53.
  10. Cogliano VJ, Baan R, Straif K, et al. Preventable exposures associated with human cancers. J Natl Cancer Inst 2011;103(24):1827-39.
  11. International Collaboration of Epidemiological Studies of Cervical Cancer. Cervical carcinoma and sexual behaviour: collaborative reanalysis of individual data on 15,461 women with cervical carcinoma and 29,164 women without cervical carcinoma from 21 epidemiological studies. Cancer Epidemiol Biomarkers Prev 2009;18(4):1060-9.
  12. Castellsagué X, Bosch FX, Muñoz N. Male circumcision, penile human papillomavirus infection, and cervical cancer in female partners. N Engl J Med 2002;346(15):1105-12.
  13. Albero G, Castellsagué X, Giuliano AR, Bosch FX. Male circumcision and genital human papillomavirus: a systematic review and meta-analysis. Sex Transm Dis 2012;39(2):104-13.
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Other factors may be associated with cervical cancer risk because they increase the risk of Human papillomavirus (HPV) exposure or persistent HPV infection (and/or may have direct effects, independent of HPV).[1]

Cervical cancer risk is almost three times higher in women who have had 6 or more sexual partners, compared with those who have had only one, a pooled analysis showed.[2] Cervical cancer risk is around doubled in women who first had sexual intercourse aged 14 or younger, compared with those who did so aged 25 or older, a pooled analysis showed.[2]

Cervical cancer risk is around halved in women whose only current male sexual partner is circumcised, compared with those whose partner is uncircumcised, a pooled analysis showed;[3] HPV prevalence is lower in circumcised versus uncircumcised men, a meta-analysis showed.[4]

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International Agency for Research on Cancer (IARC) classifies the role of this risk factor in cancer development.[1]

Cervical cancer risk is 6 times higher in women with HIV/AIDS, versus women in the general population, a meta-analysis showed.[2] Cervical cancer risk among women with HIV may be reduced by treatment with highly active antiretroviral therapy (HAART), perhaps because HAART improves immune function to support Human papillomavirus (HPV) clearance.[3-6]

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Cervical cancer risk may be further increased in women with other sexually transmitted infections (STIs) alongside human papillomavirus (HPV), a cohort study indicates.[1] This may reflect inhibited ability to clear HPV infection due to immune suppression by other STIs. Failure to detect and treat pre-cancerous lesions in women with STIs may not explain the association, as women with a history of STIs may be more likely to attend cervical screening, versus women without such a history, a cohort study showed.[2]

Cervical cancer risk in HPV-positive women is higher in those with Chlamydia trachomatis (CT), versus those without this infection.[3-5] Cervical adenocarcinoma risk is not associated with CT infection, a pooled case-control study showed.[6]

Cervical cancer risk is not associated with herpes simplex virus 2 infection, a meta-analysis showed (though some evidence of risk increase in case-control studies).[7]

References

  1. Castellsagué X, Pawlita M, Roura E, et al. Prospective seroepidemiologic study on the role of Human Papillomavirus and other infections in cervical carcinogenesis: evidence from the EPIC cohort. Int J Cancer 2014;135(2):440-52.
  2. Hansen BT, Hukkelberg SS, Haldorsen T, Eriksen T, Skare GB, Nygård M. Factors associated with non-attendance, opportunistic attendance and reminded attendance to cervical screening in an organized screening program: a cross-sectional study of 12,058 Norwegian women. BMC Public Health 2011;11:264.
  3. Castellsagué X, Pawlita M, Roura E, et al. Prospective seroepidemiologic study on the role of Human Papillomavirus and other infections in cervical carcinogenesis: evidence from the EPIC cohort. Int J Cancer 2014;135(2):440-52.
  4. Smith JS, Bosetti C, Muñoz N, et al. Chlamydia trachomatis and invasive cervical cancer: a pooled analysis of the IARC multicentric case-control study. Int J Cancer 2004;111(3):431-9.
  5. Jensen KE, Thomsen LT, Schmiedel S, et al. Chlamydia trachomatis and risk of cervical intraepithelial neoplasia grade 3 or worse in women with persistent human papillomavirus infection: a cohort study. Sex Transm Infect 2014.
  6. Castellsagué X, Díaz M, de Sanjosé S, et al. Worldwide human papillomavirus etiology of cervical adenocarcinoma and its cofactors: implications for screening and prevention. J Natl Cancer Inst 2006;98(5):303-15.
  7. Cao S, Gan Y, Dong X, Lu Z. Herpes simplex virus type 2 and the risk of cervical cancer: a meta-analysis of observational studies. Arch Gynecol Obstet 2014;290(6):1059-66.
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