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Risk Factors for Cervical Cancer

A. Modifiable Risk Factors


1. Sexual Activity
a. Early coitus
Studies have shown that the risk of cervical cancer is higher in women who had
their first sexual intercourse at 20 rather than 25 years. Although women can be infected
by HPV at any age, infections at a very young age may be especially dangerous as they
have more time to cause damage that eventually leads to cancer.
According to the WHO, the peak time for acquiring infection for both
women and men is shortly after becoming sexually active. HPV is sexually transmitted,
but penetrative sex is not required for transmission. Skin-to-skin genital contact is a well-
recognized mode of transmission.
b. Multiple sex partners
Having sex with lots of different partners increases the chances of coming into
contact with a person who is carrying the HPV virus. In other words, the probability of
encountering an infected partner increases as the number of partners a woman has
increases. Sexual activity with multiple partners also increases the likelihood of many
other sexually transmitted infections (chlamydia, gonorrhea, syphilis). Studies have found
an association between chlamydia and cervical cancer risk, including the possibility that
chlamydia may prolong HPV infection.
c. Frequent intercourse
At present, the frequency of intercourse or number of sexual act is not considered an
important part in the development of cervical cancer. Although there is some evidence
that suggests recent intercourse is associated with testing positive for HPV, these
associations are likely to reflect detection rather than true infection.

2. Sex with uncircumcised males
Men who are circumcised (have had the foreskin of the penis removed) have a lower
chance of becoming and staying infected with HPV. Men who have not been circumcised
are more likely to be infected with HPV and pass it on to their partners. The reasons for
this are unclear. It may be that after circumcision, the skin on the glans (of the penis)
goes through changes that make it more resistant to HPV infection. Another theory is that
the surface of the foreskin (which is removed by circumcision) is more easily infected by
HPV. Still, circumcision does not completely protect against HPV infection men who
are circumcised can still get HPV and pass it on to their partners.

3. Sexual contact with males whose partners have had cervical cancer
This is associated to women with multiple sexual partners. Women with sexual
contact with men whose partners have had cervical cancer may increase the risk for the
development of cervical cancer by transferring the microorganism (e.g. HPV) to other
women.

4. Early childbearing and high parity
Early child bearing is associated to early coitus. Multiparous women are at
increased risk for cervical cancer and pre cancer compared to nulliparous women,
with a progressive elevation in risk with increasing number of live births. Women
who have had 3 or more full-term pregnancies have an increased risk of developing
cervical cancer but the reason behind this still remain unknown. Increased exposure
of the transformation zone to toxic agents at birth might account for parity
association. Other studies suggest that cervical trauma during parturition might
increase the risk, an explanation compatible the observation that women who have
undergone cesarean section have a reduced risk for cervical cancer. Additional
biologic mechanisms that could explain the increased risk associated with parity
thus include hormonal changes during pregnancy or pregnancy-related
immunosuppression.

5. Smoking and exposure to second hand smoke
Biologic evidence strongly supports smokings carcinogenic effects for SCC. The
identification of tobacco-related carcinogens such as nicotine and its metabolites (e.g.
cotinine) in cervical secretions of women who smoke further support the notion that
smoking damages the DNA (genotoxicity). Smoking, it is believed, increases free radical
production and depletes antioxidants, enhancing a genotoxic-prone milieu. Smoking may
also depress local and systemic immune function, possibly increasing risk for HPV
persistence, a prerequisite for carcinogenesis. Although substantial epidemiologic and
biologic evidence now associates smoking and cervical SCC, no such equivalent
association with cervical adenocarcinoma has been found.



6. Low socioeconomic status
It has been reported that women with low socioeconomic status possess a two-fold
increase in risk for invasive cervical cancer when compared to women with high socio-
economic status are commonly defined by income and education. This association
appears similar across race and likely reflects a combination of an environmental
disposition for HPV infection, where prevalence is generally higher in women with low
socioeconomic status and where it is coupled with poor access to screening and
treatment. Though unproven, concurrent genital infections and nutritional deficiencies
may also contribute to some of the risk differences.

7. Nutritional deficiencies
The evidence for poor nutritional status and increased cervical cancer risk is sparse,
Studies have either reported protective effects or no association of high antioxidant levels
such as beta-carotene, lycopene and Vitamin E (tocopherol). Low folate levels have also
been implicated in poor DNA repair capacity and linked to increased cervical cancer risk.

8. Overweight status
Excessive fat has been shown to increase levels of estrogen and the role of estrogen is
that it stimulates cell growth and proliferation of cervical cells. Overweight women are
more likely to develop adenocarcinoma of the cervix.



B. Non-modifiable Risk Factors
1. Chronic cervical infection
a. Exposure to human papilloma virus
The most important risk factor for cervical cancer is infection by the human
papilloma virus (HPV). HPV is a group of more than 150 related viruses, some of which
cause a type of growth called a papilloma, which are more commonly known as warts.
HPV can infect cells on the surface of the skin, and those lining the genitals, anus,
mouth and throat, but not the blood or internal organs such as the heart or lungs.
HPV can be passed from one person to another during skin-to-skin contact. One
way HPV is spread is through sex, including vaginal and anal intercourse and even oral
sex.
Other types of HPV are called high-risk types because they are strongly linked to
cancers, including cancer of the cervix, vulva, and vagina in women, penile cancer in
men, and cancers of the anus, mouth, and throat in both men and women. The high-risk
types include HPV 16, HPV 18, HPV 31, HPV 33, and HPV 45, as well as some others.
There might be no visible signs of infection with a high-risk HPV until pre-cancerous
changes or cancer develops.
Doctors believe that a woman must be infected with HPV in order to develop
cervical cancer. Although this can mean infection with any of the high-risk types, about
two-thirds of all cervical cancers are caused by HPV 16 and 18.
Infection with HPV is common, and in most people the body can clear the
infection by itself. Sometimes, however, the infection does not go away and becomes
chronic. Chronic infection, especially when it is caused by certain high-risk HPV types,
can eventually cause certain cancers, such as cervical cancer.
b. Exposure to Chlamydia trachomitis
Chlamydia is a relatively common kind of bacteria that can infect the reproductive
system. It is spread by sexual contact. Some studies have seen a higher risk of cervical
cancer in women whose blood test results show evidence of past or current chlamydia
infection (compared with women who have normal test results). Women who are infected
with chlamydia often have no symptoms In fact, they may not know that they are infected
at all unless they are tested for chlamydia during a pelvic exam. Scientists at the Medical
University of South Carolina found that HPV infections last longer if Chlamydia also is
present.

2. HIV infection and other cause of immunodeficiency
Human immunodeficiency virus (HIV), the virus that causes AIDS, damages the
immune system and puts women at higher risk for HPV infections. This might explain
why women with AIDS have an increased risk for cervical cancer. The immune system is
important in destroying cancer cells and slowing their growth and spread. In women with
HIV, a cervical pre-cancer might develop into an invasive cancer faster than it normally
would. Another group of women at risk of cervical cancer are women receiving drugs to
suppress their immune response, such as those being treated for an autoimmune disease
(in which the immune system sees the body's own tissues as foreign and attacks them, as
it would a germ) or those who have had an organ transplant.




3. Family history of cervical cancer
Cervical cancer may run in some families. If the mother or sister had cervical cancer,
the chances of developing the disease are 2 to 3 times higher than if no one in the family
had it. Some researchers suspect that some instances of this familial tendency are caused
by an inherited condition that makes some women less able to fight off HPV infection
than others. In other instances, women from the same family as a patient already
diagnosed could be more likely to have one or more of the other non-genetic risk factors
previously described in this section.

References:
Robboys Pathology of the Female Reproductive Tract pp. 180-183
http://news.bbc.co.uk/2/hi/health/8420690.stm
http://umm.edu/health/medical/reports/articles/cervical-cancer
http://www.cancer.org/acs/groups/cid/documents/webcontent/003094-pdf.pdf
http://www.who.int/mediacentre/factsheets/fs380/en/