DEMONSTRATION OF SMOKING-RELATED DNA-DAMAGE IN CERVICAL EPITHELIUM AND CORRELATION WITH HUMAN PAPILLOMAVIRUS TYPE-16, USING EXFOLIATED CERVICAL CELLS

Smoking is a known aetiological risk factor for cervical cancer. Smoki ng-related DNA damage (DNA adducts), in cervical epithelial cells, has recently been demonstrated to suggest a causal role in the developmen t of cervical cancer. Human papillomavirus 16 (HPV 16) is a known onco genic virus and is also implicated as a cause of cervical cancer. It h as been suggested that both smoking and HPV may act synergistically in the development of cervical cancer. We have investigated the cervical DNA adduct level and the prevalence of HPV 16 (using polymerase chain reaction) in women who had normal cervical cytology. Both the DNA add uct assay and the HPV assay were carried out on exfoliated cervical ce lls recovered from cervical scrapes. In 87% of the cases there was eno ugh DNA from the exfoliative cervical cells to analyse for DNA adducts . Smokers had higher DNA adduct levels than non-smokers (P = 0.002), c onfirming the previous data from cervical biopsy samples. Forty-two pe r cent of the specimens were found to be HPV 16 positive. There was no significant difference in smoking-related DNA damage (DNA adduct leve ls) between HPV-positive and HPV-negative smokers. This suggests that smoking DNA damage does not augment HPV infectivity. These results do not, therefore, support the molecular synergism theory.