Langerhans' cells in cervical epithelium in colposcopic biopsy specimens were identified by immunocytochemical staining for S100 protein and T6 (CD1) antigen, and their density was quantified. Possible cofactors for the development of cervical neoplasia were examined for any effect on the cell counts per unit area. Current cigarette smoking was associated with a significant decrease in the Langerhans' cell population in both normal epithelium and lesions due to cervical intraepithelial neoplasia. Ex-smokers tended to have cell counts between those of smokers and non-smokers. There was a dose-response relation between number of cigarettes smoked daily and effect on cell counts. These findings of a local immunological effect of smoking on cervical epithelium may explain the means by which cigarette smoking contributes to the development of cervical neoplasia.
PIP: 91 women attending a colposcopy clinic in London were examined to determine whether there are local immunologic changes in the cervix associated with cigarette smoking. 36 of these women had normal cytology, normal colposcopy, and no human papilloma virus (HPV) infection or cervical intraepithelial neoplasia (CIN) in the biopsy. The remaining 55 women had both colposcopic and histologic evidence of CIN with HPV infection. Women with CIN and HPV infection had significantly lower median Langerhan's cell counts (12.1/mm2 by S100 antisera and 28.3/mm2 by T6 antisera) than women with normal findings (51.4/mm2 and 115.9/mm2, respectively). Moreover, the Langerhan's cells found in CIN/HPV lesions had fewer dendritic processes, and those present were shorter than those in normal epithelium. In areas on CIN/HPV with depleted cell counts, Langerhan's cells were confined to the region closest to the basement membrane rather than being found throughout the lower half of the epithelium as expected. Current smokers had significantly fewer Langerhan's cells in both normal epithelium (9.6 by S100, 45.4 by T6) and in CIN/HPV of all grades (7.1 by S100 and 21.6 by T6) than nonsmokers (values of 72.5 and 137.8 in normal epithelium and 25.1 and 44.5 in CIN/HPV) and ex-smokers (values of 63.6 and 115.7 in normal epithelium and 44.6 and 37.0 in CIN/HPV). This local immunologic effect of smoking on cervical epithelium may be the mechanism through which smoking promotes the development of cervical cancer.