Gynecologic oncology · 2007
Lifetime cigarette smoke and second-hand smoke and cervical intraepithelial neoplasm--a community-based case-control study.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Tsai Hsiu-Ting, Tsai Ying-Mei, Yang Sheau-Fang, Wu Kuen-Yuh, Chuang Hung-Yi, Wu Trong-Neng, Ho Chi-Kung, Lin Cheng-Chieh, Kuo Ying-Se, Wu Ming-Tsang
Аннотация
BACKGROUND: Both active cigarette smoking and human papillomavirus (HPV) infection are known risk factors for cervical intraepithelial neoplasm (CIN). The association between second-hand smoke (SHS) and CIN has not been conclusively determined. We conducted a community-based case-control study to estimate the relationship between SHS and CIN.
METHODS: Potential study subjects were selected through Pap smear screening in Kaohsiung County, Taiwan. A total of 171 subjects with either their first case of inflammation (benign epithelial lesion) or > or = CIN1 by biopsy confirmation were assigned to a case group; 513 normal subjects with negative findings by Pap smears or biopsies were assigned to a control group.
RESULTS: Non-smoking women exposed to more than 20 pack-years of cigarette smoke had a significantly greater risk of developing > or = CIN2 than unexposed non-smokers (adjusted OR=7.2, 95% CI=2.5-20.6). Among the women without HPV infections, the greater the severity of disease found in the groups (normal, inflammation, CIN1, to > or = CIN2), the more likely it was for the women to be exposed to SHS, a significant increasing trend (p=0.037).
CONCLUSIONS: In addition to HPV infection and active cigarette smoking, exposure to SHS is a major risk factor for CIN among Taiwanese women.
METHODS: Potential study subjects were selected through Pap smear screening in Kaohsiung County, Taiwan. A total of 171 subjects with either their first case of inflammation (benign epithelial lesion) or > or = CIN1 by biopsy confirmation were assigned to a case group; 513 normal subjects with negative findings by Pap smears or biopsies were assigned to a control group.
RESULTS: Non-smoking women exposed to more than 20 pack-years of cigarette smoke had a significantly greater risk of developing > or = CIN2 than unexposed non-smokers (adjusted OR=7.2, 95% CI=2.5-20.6). Among the women without HPV infections, the greater the severity of disease found in the groups (normal, inflammation, CIN1, to > or = CIN2), the more likely it was for the women to be exposed to SHS, a significant increasing trend (p=0.037).
CONCLUSIONS: In addition to HPV infection and active cigarette smoking, exposure to SHS is a major risk factor for CIN among Taiwanese women.