Epidemiological studies have shown that only a small fraction of women infected with
oncogenic HPV types will eventually progress to high-grade intraepithelial lesions
(HSIL) and cervical cancer (CC). Because infection by oncogenic HPVs is a necessary
but not a sufficient cause of CC, it has been assumed that other factors, acting in
conjunction with HPV, influence the risk of transition from cervical HPV infection
to cervical malignancy. This paper reviews the epidemiological evidence for the role
of environmental co-factors in HPV carcinogenesis as assessed from selected studies
that report associations within a well-defined HPV-DNA positive group. Co-factors
assessed include parity, use of oral contraceptives, tobacco smoking, infection with
other sexually transmitted diseases, and dietary and nutritional factors. Based on
the evidence provided by the largest epidemiological studies that using sensitive
detection methods allowed for the effects of HPV, it can be concluded that, among
HPV positive women, high parity, long-term OC use, smoking, and co-infection with
other sexually transmitted agents are the most consistently identified environmental
co-factors likely to influence the risk of progression from cervical HPV infection
to HSIL and invasive CC. There is limited evidence for a role of dietary factors in
HPV carcinogenesis. On-going epidemiological studies will shed more light into the
role of these and other co-factors, but if confirmed, these conclusions may imply
that multiparous women, women who are smokers, and women on long-term OC use, might
need a closer cytological and HPV surveillance than women in the general population.