Cigarette smoking is an established co-factor that approximately doubles the risk of cervical carcinoma. The mechanism by which smoking contributes to cervical carcinogenesis is best described as:

• A Direct conversion of tobacco carcinogens into oestrogenic metabolites within cervical epithelium
• B Chronic irritation leading to squamous metaplasia independent of any interaction with HPV
• C Induction of HPV genome integration through systemic immunodeficiency identical to that seen in AIDS
• D Concentration of nicotine-derived carcinogens in cervical mucus causing local immunosuppression and DNA damage ✓

Explanation

Smoking acts locally: nicotine derivatives such as cotinine are concentrated in cervical mucus, suppress local Langerhans cell function and generate adducts that damage DNA, synergising with persistent high-risk HPV infection. The effect is strongest for squamous cell carcinoma and is weak or absent for adenocarcinoma. Option C fails because HIV-related immunosuppression is systemic, whereas smoking exerts its main effect at the cervix itself rather than by producing AIDS-level immune paresis.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.