title: Tobacco smoking and regression of low-grade cervical abnormalities.
abstract: The role of tobacco smoking in the multistage carcinogenesis at the cervix is not fully understood because of a paucity of prospective data. To assess the relationship between smoking and spontaneous regression of cervical precursor lesions, a total of 516 women with low-grade squamous intraepithelial lesion (LSIL) were monitored by cytology and colposcopy every 4 months. Probability of LSIL regression within 2 years was analyzed in relation to smoking behaviors, with regression defined as at least two consecutive negative Pap smears and normal colposcopy. Women's age, initial biopsy results, and human papillomavirus (HPV) genotypes were included in the multivariate models for adjustments. Our study subjects included 258 never-smokers and 258 smokers (179 current and 79 former smokers). During a mean follow-up time of 39.8 months, 320 lesions regressed to normal cytology. Probability of regression within 2 years was significantly lower in smokers than in never-smokers (55.0%vs 68.8%, P = 0.004). The risk of LSIL persistence increased with smoking intensity and duration and with younger age at starting smoking (P = 0.003, P < 0.001, and P = 0.03, respectively). Smokers had twice as high a risk of persistent HPV infection compared to never-smokers (odds ratio, 2.50; 95% confidence interval, 1.30-4.81; P = 0.006). In young women, passive smoking since childhood reduced probability of regression within 2 years (56.7%vs 85.9%, P < 0.001). Further adjustments for a wide range of cervical cancer risk factors did not change the findings. In conclusion, tobacco smoking may interfere with regression of cervical precursor lesions. Childhood exposure to second-hand smoke may increase a risk of persistent cervical abnormalities among young women.
authors.affiliation: Department of Obstetrics and Gynecology, Graduate School of Comprehensive Human Science, University of Tsukuba, Tsukuba, Japan. matsumok@mui.biglobe.ne.jp
authors.forename: Koji
authors.initials: K
authors.lastname: Matsumoto
authors.forename: Akinori
authors.initials: A
authors.lastname: Oki
authors.forename: Reiko
authors.initials: R
authors.lastname: Furuta
authors.forename: Hiroo
authors.initials: H
authors.lastname: Maeda
authors.forename: Toshiharu
authors.initials: T
authors.lastname: Yasugi
authors.forename: Naoyoshi
authors.initials: N
authors.lastname: Takatsuka
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Hirai
authors.forename: Akira
authors.initials: A
authors.lastname: Mitsuhashi
authors.forename: Takuma
authors.initials: T
authors.lastname: Fujii
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Iwasaka
authors.forename: Nobuo
authors.initials: N
authors.lastname: Yaegashi
authors.forename: Yoh
authors.initials: Y
authors.lastname: Watanabe
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Nagai
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Kitagawa
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Yoshikawa
mesh_terms: D000328:Adult; D002584:Cervix Uteri / Q000473:pathology* / Q000821:virology; D003127:Colposcopy; D005260:Female; D005838:Genotype; D006801:Humans; D008875:Middle Aged; D015999:Multivariate Analysis; D065006:Papanicolaou Test; D027383:Papillomaviridae / Q000235:genetics / Q000254:growth & development; D030361:Papillomavirus Infections / Q000150:complications; D011446:Prospective Studies; D012075:Remission, Spontaneous; D018570:Risk Assessment / Q000379:methods; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*; D014028:Tobacco Smoke Pollution / Q000009:adverse effects; D002583:Uterine Cervical Neoplasms / Q000150:complications / Q000473:pathology*; D014626:Vaginal Smears; D055815:Young Adult; D002578:Uterine Cervical Dysplasia / Q000150:complications / Q000473:pathology*
chemical_list: D014028:Tobacco Smoke Pollution