Abstract

Abstract Cervical cancer is the second most common malignancy and the second most common cause of cancer-related death worldwide. Recently, the International Agency for Research on Cancer (IARC) of the World Health Organization in France completed reviewing all published studies related to cigarette smoke and cancer. Among several risk factors, tobacco smoking has been less explored despite it being a well-established risk factor for cervical precancer and cancer. The epidemiologic and biological studies suggest the association of passive smoking on the risk of cervical cancer; however, the evidence has been suggestive rather than sufficient to implicate the role of passive smoking in the etiology of cervical cancer among lifetime nonsmoking women. We investigated the associations between passive smoking and risk of cervical intraepithelial neoplasia (CIN), and cervical cancer in high risk HPV-positive women in the Korean HPV cohort study (KHPV). The KHPV recruited 1,306 women, aged 18-65, including HPV-positive women with normal cytology (n=577), CIN1 (n=419), CIN2/3 (n=165), and cervical cancer (n=145) from March 2006 to December 2009. Detailed information on passive smoking and other lifestyle factors were collected by questionnaires. Multinomial logistic analysis was performed to estimate multivariate-adjusted odds ratios. Ex- and current smoker had an increased risk of CIN1 (OR = 1.81; 95% CI: 1.26 ∼ 2.60) as compared to nonsmokers. The risk of CIN1 increased with increasing exposure time of passive smoking regardless of smoking after adjusting for potential confounder (OR = 2.09; 95% CI: 1.33 ∼ 3.28, p for trend = 0.0023). In non-smoker, the subject with passive smoking had an increased of CIN1 (OR = 1.48; 94% CI: 1.04-2.10, p for trend = 0.0276) after adjusting for potential confounder. In smoker, the effects of passive smoking were not statistically significant. Both of exposure time separated by two hours per day (p for trend = 0.0003), and 1 hour and 2 hours per day (p for trend = 0.0006) of passive smoking demonstrated significant associations with development of CIN1. This is the first study to demonstrate that passive smoking is an independent and combined risk factor of CIN1. HPV viral load and alcohol synergize to increase the risk of CIN1 among high-risk HPV-positive women. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 653. doi:1538-7445.AM2012-653

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