Cervical cancer affects the cells of the cervix, which is the lowermost part of the uterus that connects to the vagina. It is a leading cause of morbidity and mortality in women of reproductive age and post-menopause. It has been found that several factors contribute to the development of cervical cancer, chiefly among them is the human papillomavirus (HPV) and smoking.
Smoking is thought to be responsible for around 21% of all cases of cervical cancer in the UK, which has resulted in an increasing interest in the association between smoking and cervical cancer.1
This article seeks to address the link between smoking and cervical cancer, understand the mechanisms underlying this relationship and identify ways to reduce the risk and incidence of cervical cancer.
Cervical cancer is defined as a cancer of the lower female reproductive tract (the cervix) that arises due to changes in the cells. These changes take place over a prolonged period (about 10-15 years) starting from dysplasia, where the cells begin to turn abnormal, until they reach the point of neoplasia, where the cells are altered permanently, becoming cancerous and eventually spreading to involve surrounding tissues or other organs in the body. However, in individuals with compromised immune systems (for example those living with untreated human immunodeficiency virus (HIV), this time can be considerably lessened to about 5-10 years.
According to the World Health Organization, cervical cancer is currently the fourth most common cancer in women globally with around 660,000 new cases and around 350,000 related deaths in 2022. The highest rates of cervical cancer incidence and mortality are in sub-Saharan Africa (SSA), Central America and South-East Asia due to several factors, including:
People assigned female at birth (AFAB) living with HIV are six times more likely to develop cervical cancer compared to those AFAB without HIV and an estimated 5% of all cervical cancer cases are attributable to HIV.
HPV is a common sexually transmitted infection and nearly all sexually active individuals are exposed to it at some point in their lives. Fortunately, most peoples’ bodies can successfully eradicate this virus without any cause for alarm. It is the persistence of this virus and recurrent infections over a long period that ultimately lead to changes in the cervical cells.
While it has been established that infection with HPV is the strongest factor associated with the changes that occur in cervical cancer, it has also been shown that the presence of the virus alone is insufficient for the development of the disease.2
For HPV to result in cervical cancer, infection must first be with one of the high-risk types of the virus which mainly include types 16, 18, 33 and 35. These are also the strains of the virus for which vaccines have been developed.
Other risk factors have been identified and linked to the development of cervical cancer in addition to persistence of infection of HPV. These include:2
Prevention is perhaps the most important public health strategy due to the high rates of morbidity and mortality associated with cervical cancer.
In order to protect those at risk of the disease, different vaccines against HPV have been developed to be administered to girls aged 9-14 years. In some countries (e.g. Australia, the US, UK and many EU countries) the vaccine is also administered to boys in the same age group to ensure there is no transmission of HPV. This vaccine has been found to be effective in preventing infection with HPV and ultimately preventing cervical cancer.3 There are currently six licensed HPV vaccines.
Screening of the health of the cervix is also widely advocated for women of reproductive age. This is done by means of a special test called cervical screening (formerly known as a smear test in the UK) which checks a small sample of cells of the cervix for specific, “high-risk” types of HPV, which can cause changes to the cells of the cervix. If tests find these types of HPV to be present, the sample is then checked for any changes to the cells of the cervix. These abnormal cells can then be treated early and progression to cancer can be halted.
In the UK, cervical screening is offered to all women and people with a cervix aged between 25 and 64. Frequency of screening is as follows:
Other means of cervical cancer prevention include:
Additionally, awareness campaigns on the dangers of cervical cancer and the importance of HPV vaccination and screening should also be taken into consideration.
Numerous studies have consistently shown a positive association between smoking and cervical cancer risk. A meta-analysis (a statistical analysis of the results of multiple studies) of twenty-four case-control studies found that current smokers had a 2.1-fold increased risk of cervical cancer compared to non-smokers.4
Another study found that smoking status, duration and intensity showed a two-fold increased risk of cervical cancer, while time since quitting was associated with a two-fold reduced risk.5 Although there is not enough research, it has also been proposed that even secondhand or passive smoking significantly increases the risk of developing cervical cancer.
Smoking has been linked as the causative factor for a number of cancers due to the carcinogenic (cancer-causing) nature of tobacco. The risk of cervical cancer increases with the number of years smoked and the amount of cigarettes smoked per day.6
Tobacco contains compounds such as polycyclic aromatic hydrocarbons (PAHs) and volatile organic compounds (VOCs) which are believed to damage DNA, disrupt immune function and promote the growth of cancer cells.
The mechanisms through which smoking results in cervical cancer are as follows:
Cessation of smoking has been shown to reduce the risk of cervical cancer. In some cases, it has helped to reduce the risk of recurrence of pre-malignant changes and, eventually, the restoration of the cervical cells to normal.8 It has also been found that by reducing the number of times a person smokes, there is a concurrent reduction in the severity of the cervical changes and the recurrence.
As such, there is a need to emphasise the importance of tobacco control measures in the prevention of cervical cancer. Public health interventions aimed at reducing smoking prevalence, such as tobacco taxation, smoking cessation programs, and comprehensive smoke-free policies, can have significant impacts on cervical cancer incidence and mortality. Additionally, targeted education campaigns emphasising the role of smoking in cervical cancer development can raise awareness and encourage behaviour change among at-risk populations, particularly young women.
